Academic literature on the topic 'Arterial pressure. eng'
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Journal articles on the topic "Arterial pressure. eng"
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Belyayeva, V. A. "The impact of meteo-factors on increase of arterial blood pressure." Health Risk Analysis, no. 4 (April 2016): 17–22. http://dx.doi.org/10.21668/health.risk/2016.4.02.eng.
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Coral-Alvarado, Paola Ximena, Maria Fernanda Garces, Jorge Eduardo Caminos, Antonio Iglesias-Gamarra, José Félix Restrepo, and Gerardo Quintana. "Serum Endoglin Levels in Patients Suffering from Systemic Sclerosis and Elevated Systolic Pulmonary Arterial Pressure." International Journal of Rheumatology 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/969383.
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Background. Pulmonary arterial hypertension (PAH) is the main cause of morbimortality in systemic sclerosis (SSc). Increased Eng expression has been demonstrated in SSc patients.Objective. Ascertaining serum levels of Eng in SSc patients with and without elevated systolic pulmonary arterial pressure (sPAP) and comparing them with that of healthy volunteers.Methods. A cross-sectional study was carried out. A commercial ELISA kit was used for measuring serum concentrations of Eng in 60 subjects: 40 patients with SSc with and without elevated sPAP, compared to 20 healthy control subjects. Elevated sPAP was detected by echocardiogram.Results. No association between positive Eng and elevated sPAP was found when compared to the SSc without elevated sPAP group (OR=2.85; 0.65–12.88 95% CI;P=.11); however, an association was found between positive Eng and elevated sPAP compared to healthy controls (OR=23.22; 2.46–1050.33 95% CI;P=.001), and weak association was found between the positive Eng with SSc without elevated sPAP group compared to healthy controls (OR=8.14, 0.8–393.74 95% CI;P=.046).Conclusion. Raised serum levels of Eng in SSc patients compared to healthy controls were found, suggesting a role for Eng in SSc vasculopathy and not just in elevated sPAP. However, prospective studies are needed to verify such observations.
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Tas, Umit, and Ahmet Akbas. "ANFIS Based Modeling of the Hormonal Effects of GLP-2 on the Mean Arterial Pressure and Blood Volume of Rats." مجلة جامعة الملك عبدالعزيز-العلوم الهندسية 25, no. 1 (2014): 21–32. http://dx.doi.org/10.4197/eng.25-1.2.
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Umnyagina, I. A., T. V. Blinova, L. A. Strakhova, V. V. Troshin, Yu V. Ivanova, and E. I. Sorokina. "Endothelin-1 as a risk factor causing cardiovascular pathology in young and middle-aged people employed under hazardous working conditions." Health Risk Analysis, no. 2 (June 2021): 105–13. http://dx.doi.org/10.21668/health.risk/2021.2.10.eng.
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Our research goal was to reveal peculiarities related to changes in endothelin-1 contents in blood serum in young and middle-aged people exposed to occupational noise and industrial welding and silicon-containing aerosols with fibrogenic effects. Another goal was to establish a correlation between endothelin-1 contents and blood pressure, body mass, and dyslipidemia. We examined workers employed at a metallurgic plant in Nizhniy Novgorod region. Endothelin-1 concentration in blood serum was determined with «Endothelin (1-21)», a reagent kit for ELISA produced by «Biomedica Medizinprodukte GmbH & Co KG» (Austria). We detected certain group differences in endothelin-1 contents in blood serum and frequency of its elevated concentrations between workers who had to work under different working conditions. We established a direct correlation between endothelin-1 and blood pressure, total cholesterol, and body mass index. Elevated endothelin-1 contents in people suffering from arterial hypertension can indicate a higher risk of complications this disease might have. People who have elevated endothelin-1 contents but normal blood pressure, total cholesterol within physiological standard and normal body mass index can be recommended to have regular medical check-ups focusing on functional state of their cardiovascular system; endothelin-1 in this case should be considered a risk factor that might cause cardiovascular pathology occurrence. An individual approach is required when assessing elevated endothelin-1 contents and probable use of this parameter as a risk factor that might cause cardiovascular pathology in young and middle-aged people employed under hazardous working conditions.
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Weese-Mayer, D. E., R. T. Brouillette, L. Klemka, and C. E. Hunt. "Effects of almitrine on hypoglossal and phrenic electroneurograms." Journal of Applied Physiology 59, no. 1 (July 1, 1985): 105–12. http://dx.doi.org/10.1152/jappl.1985.59.1.105.
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Almitrine increases breathing by stimulating peripheral chemoreceptors. Previous studies suggest clinical usefulness in the adult with chronic obstructive pulmonary disease, but little data are available to decide whether almitrine would be helpful in diseases involving pharyngeal airway obstruction, such as apnea of prematurity or obstructive sleep apnea. We investigated the effect of intravenous almitrine on hypoglossal (HG), an upper airway nerve, and phrenic (PHR) neural activity in eight alpha-chloralose-urethan anesthetized, paralyzed, vagotomized, and artificially ventilated cats. Recordings were made of raw and integrated HG and PHR electroneurograms (ENGs), alveolar PCO2, arterial PO2, arterial blood pressure, and rectal temperature. A dose-response study of cumulative almitrine doses ranging from 0.1 to 4.0 mg/kg was performed in three cats. The interactive effects of almitrine and hypoxic stimulation were investigated in four cats. The interactive effects of almitrine and hypercapnic stimulation were investigated in five cats. The interactive effects of almitrine and ventilatory timing were investigated in six cats. We found that 1) almitrine doses as low as 0.1 mg/kg iv increased both HG and PHR ENG activity, with a maximum effect at approximately 1.0 mg/kg; 2) almitrine markedly increased HG and PHR ENG activity at all arterial PO2 values from 35–175 Torr; 3) almitrine increased HG and PHR ENG activity at all arterial PCO2 values from 30–70 Torr; and 4) almitrine increased the ratio of tidal volume to inspiratory time and decreased the inspiratory muscle duty cycle at normoxia and eucapnia.
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Tsamis, Alkiviadis, and Nikos Stergiopulos. "Arterial remodeling in response to hypertension using a constituent-based model." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 5 (November 2007): H3130—H3139. http://dx.doi.org/10.1152/ajpheart.00684.2007.
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Hypertension-induced arterial remodeling has been previously modeled using stress-driven remodeling rate equations in terms of global geometrical adaptation (Rachev A, Stergiopulos N, Meister JJ. Theoretical study of dynamics of arterial wall remodeling in response to changes in blood pressure. J Biomech 29: 635–642, 1996) and was extended later to include adaptation of material properties (Rachev A, Stergiopulos N, Meister JJ. A model for geometric and mechanical adaptation of arteries to sustained hypertension. J Biomech Eng 120: 9–17, 1998). These models, however, used a phenomenological strain energy function (SEF), the parameters of which do not bear a clear physiological meaning. Here, we extend the work of Rachev et al. (1998) by applying similar remodeling rate equations to a constituent-based SEF. The new SEF includes a statistical description for collagen engagement, and remodeling now affects material properties only through changes in the collagen engagement probability density function. The model predicts asymptotic wall thickening and unchanged deformed inner radius as to conserve hoop stress and intimal shear stress, respectively, at the final adapted hypertensive state. Mechanical adaptation serves to restore arterial compliance to control levels. Average circumferential stress-strain curves show that the material at the final adapted hypertensive state is softer than its normotensive counterpart. These findings as well as the predicted pressure-diameter curves are in good qualitative agreement with experimental data. The novelty in our findings is that biomechanical adaptation leading to maintenance of compliance at the hypertensive state can be perfectly achieved by appropriate readjustment of the collagen engagement profile alone.
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Fan, Wei, and Michael C. Andresen. "Differential frequency-dependent reflex integration of myelinated and nonmyelinated rat aortic baroreceptors." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 2 (August 1, 1998): H632—H640. http://dx.doi.org/10.1152/ajpheart.1998.275.2.h632.
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Electrical activation of myelinated (A type) and nonmyelinated (C type) baroreceptor axons (BR) in aortic depressor nerve (ADN) evoked baroreflex changes in mean arterial pressure (MAP) in chloralose-urethan-anesthetized rats. Low stimulation intensities (<3 V) activated only A-type BR electroneurograms (ENG). A-type selective stimulus trains required minimum frequencies >10 Hz to evoke reflex MAP decreases, and the largest MAP responses occurred at 50 Hz and higher. In contrast, high stimulation intensities (18–20 V) maximally activated two volleys in ADN ENG corresponding to A- and C-type BR volleys. High-intensity trains decreased MAP at low frequency (1 Hz) and largest reflex responses at ≥5 Hz. Capsaicin (Cap) applied periaxonally to ADN selectively blocked C-type ENG volleys but not A-type volleys. Reflex curves with supramaximal intensity during Cap were indistinguishable from the pre-Cap, low-intensity baroreflexes. In comparison, vagus ENG showed graded Cap block of the C-fiber volley (ED50 = 200 nM) without significant attenuation of the A-type volley below 1 μM. However, 100 μM Cap blocked conduction in all myelinated vagal axons as well as C-type axons. Thus Cap is selective for sensory C-type axons only at low micromolar concentrations. Myelinated and nonmyelinated arterial BR evoke characteristically different frequency-response reflex relations that suggest distinct differences in sensory information processing mechanisms.
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SARIFUDDIN, SANTABRATA CHAKRAVARTY, and PRASHANTA KUMAR MANDAL. "EFFECT OF ASYMMETRY AND ROUGHNESS OF STENOSIS ON NON-NEWTONIAN FLOW PAST AN ARTERIAL SEGMENT." International Journal of Computational Methods 06, no. 03 (September 2009): 361–88. http://dx.doi.org/10.1142/s0219876209001887.
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Numerical investigations of non-Newtonian blood flow are carried out through an asymmetric arterial constriction (stenosis) obtained from casting of mildly stenosed artery [Back et al. [1984] Effect of mild atherosclerosis on flow resistance in a coronary artery casting by man, J. Biomech. Eng., Trans. ASME106, 48]. The Marker and Cell method, for governing equations of motion for the flow in primitive variables formulations is developed in a staggered grid to discretize the momentum equations representing the non-Newtonian viscous incompressible flow characterized by the generalized Power-law model in cylindrical coordinates system under axial symmetric conditions so that the problem effectively becomes two-dimensional. The modified pressure equation has been solved by Successive-Over-Relaxation method and the pressure–velocity correction formulae have been derived. Satisfactory level of convergence namely, the mass conservation of the order of 0.5 × 10-12 and consequently the steady-state criteria have been achieved. The separation points, reattachment points, pressure drop, and the wall shear stress distribution resulting from the present simulation agree well with the available numerical and experimental results. Secondary separation has also been predicted at higher Reynolds numbers. Further, in-depth study of the flow patterns reveals that shear-thickening model of generalized Power-law fluid experiences excess pressure drop more than that of shear-thinning model as in the case of flow past through cosine and smooth-shaped constrictions than irregular ones. The efficiency of the numerical code is illustrated by applying it to a test problem in order to validate the applicability of the technique as well as the simulation under consideration.
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Bofarid, Sala, Anna E. Hosman, Johannes J. Mager, Repke J. Snijder, and Marco C. Post. "Pulmonary Vascular Complications in Hereditary Hemorrhagic Telangiectasia and the Underlying Pathophysiology." International Journal of Molecular Sciences 22, no. 7 (March 27, 2021): 3471. http://dx.doi.org/10.3390/ijms22073471.
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In this review, we discuss the role of transforming growth factor-beta (TGF-β) in the development of pulmonary vascular disease (PVD), both pulmonary arteriovenous malformations (AVM) and pulmonary hypertension (PH), in hereditary hemorrhagic telangiectasia (HHT). HHT or Rendu-Osler-Weber disease is an autosomal dominant genetic disorder with an estimated prevalence of 1 in 5000 persons and characterized by epistaxis, telangiectasia and AVMs in more than 80% of cases, HHT is caused by a mutation in the ENG gene on chromosome 9 encoding for the protein endoglin or activin receptor-like kinase 1 (ACVRL1) gene on chromosome 12 encoding for the protein ALK-1, resulting in HHT type 1 or HHT type 2, respectively. A third disease-causing mutation has been found in the SMAD-4 gene, causing a combination of HHT and juvenile polyposis coli. All three genes play a role in the TGF-β signaling pathway that is essential in angiogenesis where it plays a pivotal role in neoangiogenesis, vessel maturation and stabilization. PH is characterized by elevated mean pulmonary arterial pressure caused by a variety of different underlying pathologies. HHT carries an additional increased risk of PH because of high cardiac output as a result of anemia and shunting through hepatic AVMs, or development of pulmonary arterial hypertension due to interference of the TGF-β pathway. HHT in combination with PH is associated with a worse prognosis due to right-sided cardiac failure. The treatment of PVD in HHT includes medical or interventional therapy.
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Bouwmeester, J. Christopher, Israel Belenkie, Nigel G. Shrive, and John V. Tyberg. "Partitioning pulmonary vascular resistance using the reservoir-wave model." Journal of Applied Physiology 115, no. 12 (December 15, 2013): 1838–45. http://dx.doi.org/10.1152/japplphysiol.00750.2013.
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The conventional determination of pulmonary vascular resistance does not indicate which vascular segments contribute to the total resistance of the pulmonary circulation. Using measurements of pressure and flow, the reservoir-wave model can be used to partition total pulmonary vascular resistance into arterial, microcirculation, and venous components. Changes to these resistance components are investigated during hypoxia and inhaled nitric oxide, volume loading, and positive end-expiratory pressure. The reservoir-wave model defines the pressure of a volume-related reservoir and the asymptotic pressure. The mean values of arterial and venous reservoir pressures and arterial and venous asymptotic pressures define a series of resistances between the main pulmonary artery and the pulmonary veins: the resistance of large and small arteries, the microcirculation, and veins. In 11 anaesthetized, open-chest dogs, pressure and flow were measured in the main pulmonary artery and a single pulmonary vein. Volume loading reduced each vascular resistance component, whereas positive end-expiratory pressure only increased microcirculation resistance. Hypoxia increased the resistance of small arteries and veins, whereas nitric oxide only decreased small-artery resistance significantly. The reservoir-wave model provides a novel method to deconstruct total pulmonary vascular resistance. The results are consistent with the expected physiological responses of the pulmonary circulation and provide additional information regarding which segments of the pulmonary circulation react to hypoxia and nitric oxide.
Dissertations / Theses on the topic "Arterial pressure. eng"
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Cunha, Marcos Guimarães de Souza. "Análise do fluxo sanguíneo da artéria braquial em diferentes pressões no manguito do esfigmomanômetro /." Guaratinguetá : [s.n.], 2003. http://hdl.handle.net/11449/97138.
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Orientador: Araildo Lima da SilvaBanca: Carlos Renato Zacharias
Banca: Clifford Neves Pinto
Resumo: O presente trabalho consiste no estudo do comportamento do fluxo sangüíneo na artéria braquial, através de sinais captados por um microfone acoplado no estetoscópio e utilizado para transformar o sinal acústico (sonoro) em elétrico, e enviá-lo para o computador. O estudo foi realizado oferecendo-se diferentes pressões no esfigmomanômetro, o qual foi adaptado com dois manômetros. Um dos manômetros, graduado em mmHg, não foi modificado, possui o selo do INMETRO e atuou como referência, ao outro foi inserido um extensômetro, que transformou o sinal de pressão em sinal elétrico, utilizando uma ponte amplificada, enviando-o para uma placa de aquisição de dados no computador. Foi traçada uma curva de calibração do sinal elétrico (em mV) com relação ao manômetro graduado em mmHg. Foi proposto um protocolo para aquisição destes sinais a serem analisados, baseado em protocolos de aferição de pressão arterial. O comportamento do fluxo sangüíneo foi comparado às diferentes pressões exercidas pelo esfigmomanômetro. Ao analisar estes dados, foram propostos limites de normalidades da intensidade do sinal do fluxo sangüíneo em diferentes freqüências nas cinco fases da escala de Koroktov. O trabalho mostrou também os limites de normalidade da pressão arterial, utilizando-se o sinal adquirido pela extensometria. Finalmente, foi oferecido mais um auxílio no diagnóstico de patologias do sistema cardiovascular.
Abstract: The present work consists to study the features of blood flow in to the brachial artery through signals detected by a microphone coupled together a stethoscope. This apparatus changes the acoustics in eletric signal and, then, sends to the computer. This study was implemented exhibiting different pressures in the sphygnomanometer, where two manometers, graded in mmHg, were coulpled. One that has the INMETRO certificate of gauging instruments was not modificate and, then, it was used as the standard. In the other, an extensometer was coupled together, which through an amplifier bridge, pressure signals are transformed in electric signals and sent to a data adapter unit connected to the computer. A gauging curve for the eletric signals versus pressure signals was ploted. It was proposed a protocol to adquire these data signals, based on the protocol of brachial pressure measurement. The features of blood flow were compared at different sphygnomanometer pressures. In the analysis process of the data, normality boundaries of intensity were proposed to the blood flow signal at different frequencies in the five phases of the Koroktov scale. The work also showed the normality boundaries of brachial pressure using the data signals adquired by the extensometry process. Finally, it was provided an one more aid in to diagnose pathologies in the cardiovascular system.
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Moro, Juliana Vitti. "Efeitos cardiovasculares e respiratórios da infusão contínua ne naloxona ou tramadol, em coelhos anestesiados com isofluorano e submetidos à hipovolemia aguda /." Jaboticabal : [s.n.], 2009. http://hdl.handle.net/11449/89083.
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Orientador: Newton NunesBanca: Paulo Sérgio Patto dos Santos
Banca: Celina Tie Nishimori Duque
Resumo: Para avaliar os efeitos da infusão contínua de naloxona ou tramadol sobre a resposta à hipovolemia aguda foram utilizados 40 coelhos adultos distribuídos em cinco grupos: grupo naloxona (GN), grupo tramadol 1 (GT1), grupo tramadol 3 (GT3), grupo tramadol 5 (GT5) e grupo controle (GC). Os animais foram induzidos (2,5 CAM) e mantidos (1,5 CAM) à anestesia com isofluorano e após 60 minutos receberam bolus de solução de NaCl a 0,9% (GC), de naloxona (GN) ou de diferentes doses de tramadol (GT1, GT3 e GT5), seguido de infusão contínua dos mesmos fármacos. Decorridos dez minutos, os coelhos foram induzidos à hipovolemia por meio da retirada de sangue arterial no volume total de 15 ml/kg, o qual foi reinfundido após uma hora. Os parâmetros avaliados foram frequência cardíaca, eletrocardiografia, pressão venosa central, pressões arteriais (PA), pressão de perfusão coronariana (PPC), frequência respiratória, saturação de oxiemoglobina e tensão parcial de dióxido de carbono ao final da expiração. Os dados foram submetidos à análise de variância seguida pelo teste de Tukey (p<0,05). Houve diminuição significativa das médias de PA e PPC após a retirada sanguínea, em todos os grupos, com posterior retorno aos valores iniciais durante a reinfusão do sangue, com exceção do GT5 que apresentou médias estáveis durante a hipovolemia e reinfusão. O GC e GT1 apresentaram médias de PA e PPC menores que as do GT5 vinte minutos após a remoção sanguínea. As demais variáveis não apresentaram diferença significativa ao longo do período experimental. Concluiu-se que a administração do tramadol, na dose de 5 mg/kg seguida por infusão contínua de 0,025 mg/kg/min, é indicada na terapia da hipovolemia aguda, pois possui ações benéficas na PA e na PPC, sem alterar os demais parâmetros estudados.
Abstract: To evaluate the effects of continuous infusion of naloxone or tramadol on the answer to acute hypovolemia, forty adult rabbits were assigned into five groups: naloxone group (NG), tramadol group 1 (TG1), tramadol group 3 (TG3), tramadol group 5 (TG5) and control group (CG). General anesthesia was induced (2.5 CAM) and maintained (1.5 CAM) with isoflurane and, after sixty minutes, the bolus of NaCl to 0.9% (CG), of naloxone (NG) or the several doses of tramadol (TG1, TG3 e TG5) followed by continuous infusion of the same drugs were administered. After 10 minutes, the rabbits were induced to hypovolemia by withdrawing arterial blood in total volume of 15 ml/kg, which was reinfused after one hour. Heart rate, electrocardiogram, venous central pressure, arterial pressures (AP), coronary perfusion pressure (CPP), respiratory rate, pulse oxygen saturation and end-tidal carbon dioxide were evaluated. Numerical data were submitted to analyses of variance followed by Tukey test (p<0.05). The AP and CPP decreased significantly, after blood withdrawal, in all groups. During blood reinfusion, these parameters came back to the initial values, except in TG5, because these variables were stable during hypovolemia and blood reinfusion. The CG and TG1 showed mean of AP and CPP lower than the TG5 at twenty minutes after the withdrawal of blood. It was concluded that tramadol administration, at dose of 5 mg/kg followed by continuous infusion of 0.025 mg/kg/min, is indicated in therapy of acute hypovolemia, because it has useful action on AP and on CPP, besides this drug does not impair the other evaluated parameters.
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Champion, Tatiana. "Efeitos da obesidade e do sobrepeso sobre parâmetros cardiovasculares e respiratórios em gatos /." Jaboticabal : [s.n.], 2011. http://hdl.handle.net/11449/101245.
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Orientador: Aparecido Antonio CamachoBanca: Aulus Cavalieri Carciofi
Banca: Glaucia Bueno Pereira Neto
Banca: José Alberto Montoya Alonso
Banca: Julio Carlos Canola
Resumo: O estudo caracterizou a influência da obesidade e do sobrepeso sobre parâmetros cardiovasculares em gatos. Foram estudados 15 gatos obesos, sete com sobrepeso e sete com escore de condição corporal ideal. Não foram evidenciadas alterações laboratoriais compatíveis com estímulo do sistema renina angiotensina-aldosterona. Verificou-se a ocorrência pressão arterial sistólica acima de 150mmHg em 73,33% dos animais obesos, com nítido aumento (p < 0,0001) da PAS no grupo obeso, comparado aos grupos sobrepeso e com ECC ideal. O aumento da PAS foi acompanhado de disfunção diastólica, havendo correlação da PAS com a relação E/A do fluxo mitral (p = 0,0008, r = -0,40), além de maiores valores de espessura da parede livre e do septo interventricular na diástole (p<0,05). À avaliação radiográfica, não foram verificadas diferenças no VHS e distância precordial, apenas maiores valores da mensuração da gordura falciforme nos animais obesos. Com relação às anormalidades eletrocardiográficas, houve maior ocorrência de arritmias ventriculares complexas ao Holter de 24 horas dos gatos obesos (p<0,05). O ritmo predominante na eletrocardiografia computadorizada foi sinusal, enquanto no Holter de 24 horas, foi arritmia sinusal em todos os grupos. Não houve diferenças entre as frequências cardíacas entre os grupos, tampouco variação circadiana. Também não se observaram diferenças entre os períodos em bradicardia ou taquicardia e entre os índices de variabilidade da frequência cardíaca no domínio do tempo. Na avaliação respiratória, animais obesos anestesiados apresentaram menores volumes correntes e VCO2 (p<0,05) além da tendência à hipoxemia. Gatos em sobrepeso também apresentaram menores valores de PaO2, porém sem alterações na ventilometria ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: This study aimed to characterize the influence of obesity and overweight on cardiovascular parameters in cats. Twenty nine cats were evaluated (15 obese, seven overweight and seven with ideal ECC). There were no differences on parameters that reflect increase of aldosterone-angiotensin renin activity in obese cats. Systolic blood pressure was higher than 150mmHg in 73.33% of obese animals with a marked increase in systolic blood pressure (p < 0,0001) in obese group, compared to overweight or cats with ideal ECC. The increase in systolic blood pressure was accompanied by diastolic dysfunction, evidenced by the correlation (p = 0.0008, r = -0.40) with the E/A ratio of mitral flow. Moreover, obese animals had higher values of free wall thickness and interventricular septum in diastole (p<0,05). At radiographic evaluation, there were no differences in VHS, precordial distance and chest depth, only higher values of falciform fat in the obese animals. Regarding electrocardiographic abnormalities, in 24-Holter of obese cats, it was found a higher occurrence of complexes ventricular arrhythmias. The predominant rhythm in computerized ECG was sinus rhythm, while in the 24-hour Holter was sinus arrhythmia in all groups. There was no difference between heart rate throughout the day, either between the groups. Also, there were no differences in the periods of bradycardia or tachycardia and in the indexes of heart rate variability in the time domain between groups. Regarding the respiratory evaluation, anesthetized obese cats showed lower tidal volumes and VCO2 (p<0,05) and obese and overweight cats showed a tendency to hypoxemia. Therefore, obesity can cause changes on cardiorespiratory parameters, proportionally to increase of body weight and body fat
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Brum, Alexandre Martini de. "Avaliação da função renal de cães sadios e nefropatas crônicos sob diferentes bloqueios medicamentosos do sistema renina-angiotensina-aldosterona /." Jaboticabal : [s.n.], 2011. http://hdl.handle.net/11449/101235.
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Orientador: Marileda Bonafim CarvalhoBanca: Mácia Mery Kogika
Banca: Sandra Regina Ribeiro da Silva
Banca: Mirela Tinucci Costa
Banca: Áureo Evangelista Santana
Resumo: A função renal está sob influência de diversos hormônios, entre eles podemos citar o sistema renina-angiotensina-aldosterona (SRAA), que possui importante papel na manutenção do volume circulante e equilíbrio eletrolítico, entretanto também está relacionado com a progressão da doença renal. Entre seus efeitos deletérios, pode-se citar a hipertensão arterial e glomerular, proteinúria e glomeruloesclerose. Em Medicina, o tratamento medicamentoso da doença renal crônica consiste na utilização de inibidores da enzima conversora da angiotensina (iECA), antagonistas dos receptores da angiotensina II (ATAII) e/ou antagonistas da aldosterona, na forma de bloqueios simples, duplo ou triplo. Entretanto, somente o primeiro grupo de medicamentos é utilizado em Medicina Veterinária. Para testar a hipótese, que os bloqueios duplos e triplos possam beneficiar animais portadores de DRC, o presente estudo teve como objetivo avaliar a função renal de cães sadios e nefropatas submetidos a protocolos diferentes de inibição do SRAA. Os animais foram submetidos a terapias isoladas ou combinadas com cloridrato de benazepril, losartan potássico e espironolactona, durante sete dias, sendo avaliados no último dia. As avaliações consistiam em bioquímica sérica, urinálise, U-P/C, Ccr, metabolismo do sódio e potássio, além da PAS. Nos cães sadios, as terapias com benazepril (isolado ou associado) induziram aumento da concentração sérica de potássio, enquanto os bloqueios, duplo e triplo, reduziram a PAS. Nos nefropatas, todas as terapias reduziram a proteinúria, enquanto as terapias associadas reduziram a PAS e a excreção renal de potássio
Abstract: The renal function is under several hormones, like reninangiotensin- aldosterone system (RAAS), that have an important hole in the control of extravascular volume and electrolytic balance, however is related in the progression of renal disease, with proteinuria, glomerular hyperfiltration and glomerulosclerosis. In Medicine, the medical treatment of chronic renal failure consists in the use of ACE inhibitors, angiotensin II receptors antagonists (AIIRA) and/or aldosterone antagonists, however, only the first group is used in Veterinary Medicine. To prove the hypothesis that double or triple blockade can benefits animals with CRD, this study was conducted to evaluate the renal function of healthy dogs under different protocols of inhibition of RAAS. The dog received isolated ou associated therapies with benazepril, losartan and espironolactone, for seven days, with evaluation on the seventh Day. The evaluations consisted in serum biochemistry, urinalisis, UPC, Ccr, sodium and potassium metabolism, and SAP. In the healthy dog, the therapy with benazepril (isolated or associated) increased serum potassium levels, while the blockaded, duple or triple, decreased SAP. In nephropatic dogs, all therapies decreased proteinuria, while associated therapies decreased SAP and renal excretion of potassium
Doutor
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Zago, Anderson Saranz. "Avaliação gênica da sintase de óxido nítrico endotelial (eNOS) em adultos de mesma idade e idosos hipertensos submetidos ao treinamento físico : efeito na pressão arterial /." Rio Claro : [s.n.], 2007. http://hdl.handle.net/11449/100435.
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Orientador: Eduardo KokubunBanca: Cláudio Alexandre Gobatto
Banca: Eliete Luciano
Banca: Sandra Lia do Amaral
Banca: Ricardo Jacó de Almeida
Resumo: Uma alta incidência de hipertensão arterial, que possui uma etiologia multifatorial envolvendo fatores genéticos, ambientais e psicológicos, tem sido observada na população mundial. Desta forma o entendimento dos mecanismos celulares e moleculares envolvidos na gênese da hipertensão arterial é fundamental para se alcançar medidas preventivas e terapêuticas para o controle da pressão arterial. O óxido nítrico (NO) produzido pelas células endoteliais assume um importante papel no controle cardiovascular, pois tem sido considerado ser um potente vasodilatador e regulador da pressão arterial. Entretanto, as disfunções endoteliais, caracterizadas pela baixa produção e/ou biodisponibilidade do NO e alguns fatores genéticos (polimorfismos), podem contribuir para o surgimento da hipertensão arterial. Assim, o objetivo deste estudo foi investigar a influência de um programa de exercício aeróbio nas concentrações e biodisponibilidade de NO em portadores do polimorfismo T-786C do gene da eNOS e verificar o efeito dessas variáveis na pressão arterial. O DNA dos participantes foi isolado das células mononucleares periféricas e o diagnóstico genético foi realizado pela técnica de PCR. As análises de concentrações de NO, atividade da superóxido dismutase (SOD), pressão arterial, fluxo sanguíneo, composição corporal (índice de massa corporal e porcentagem de gordura corporal), perfil lipídico (colesterol total, LDL-colesterol, HDL-colesterol e triglicerídeos) e glicemia foram analisadas antes de após 6 meses de um programa de exercício físico aeróbio (70% do VO2 max) em adultos de meia idade e idosos subdivididos de acordo com a genotipagem o nível inicial de pressão arterial. Os resultados mostraram que as variáveis do perfil lipídico não exerceram nenhuma influência na relação entre hipertensão, concentrações de NO e polimorfismo do gene da eNOS... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Hypertension has a high incidence in the population of the world and its etiology is multifatorial, involving genetic, environmental and psychological factors. Understanding of the cell and molecular mechanisms involved in the genesis of hypertension is fundamental for the attainment of preventive and/or therapeutic measures for blood pressure control. Nitric Oxide (NO) produced by the endothelial cells has a particularly important role in cardiovascular control because it is a potent vasodilator and thus its role in blood pressure control is extremely relevant. However, the endothelial dysfunction which is characterized by a lower production and/or NO bioavailability, and some genetic factors can contribute to the genesis of hypertension. Therefore, the purpose of this study was investigate the influence of aerobic exercise training (AEX) on the NO concentration and bioavailability in 786C allele carriers and verify the effect of theses variable on the blood pressure. Genomic DNA was isolated from peripheral mononuclear cells and genotyping was done by standard PCR methods. The NOx assay, SOD activity, casual blood pressure, blood flow, body composition (body mass index and body fat), and lipid profile (cholesterol, LDL-cholesterol, HDLcholesterol, glucose, and triglycerides) was evaluated before and after 6 months of AEX (70% of VO2 max) in adults and elderly divided in groups according genotype and blood pressure levels. The results showed that there is no interference of lipid profile on the relationship among hypertension, NO concentration and eNOS polymorphism and the body composition variables showed a small interference on this relationship. NOx levels was associated with blood pressure values and NOx levels were significantly lower in the TC+CC group compared to the TT group at baseline... (Complete abstract click electronic access below)
Doutor
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Lima, Cláudia Gonçalves de. "Atividade protetora cardiovascular do suco de laranja vermelha em indivíduos adultos /." Araraquara : [s.n.], 2010. http://hdl.handle.net/11449/88631.
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Orientador: Thais Borges CésarBanca: Magali C. Monteiro da Silva
Banca: Lívia Gussoni Basile
Resumo: Este estudo teve como objetivo investigar a ingestão regular do suco de laranja de polpa vermelha sobre alguns fatores de risco para o desenvolvimento de doenças cardiovasculares em indivíduos adultos residentes nos municípios de Araraquara (SP) e Matão (SP). A variedade das laranjas de polpa vermelha é também conhecida como laranja sanguínea de Mombuca, e sua coloração é devida à presença de carotenóides, especialmente beta-caroteno e licopeno. Participaram deste estudo 19 homens e 16 mulheres que receberam 750 mL/dia de suco de laranja vermelha pasteurizado durante 8 semanas. As variáveis antropométricas utilizadas foram: peso, altura, dobras cutâneas do tríceps, bíceps, subescapular e suprailíaca e circunferência da cintura. Para a avaliação bioquímica foram realizadas dosagens de colesterol total, colesterol de HDL, apolipoproteínas A1 e B, proteína C reativa, homocisteína, triglicérides e glicemia. Para a avaliação hemodinâmica foram verificadas a pressão arterial sistólica e a diastólica, e para a avaliação dietética foi utilizado o recordatório alimentar de 24 horas. Todas as avaliações foram realizadas antes e após o consumo de suco de laranja vermelha. Os resultados mostraram que o colesterol total foi reduzido em 9% entre os participantes que consumiram o suco de laranja vermelha, o colesterol de LDL em 11%, a apolipoproteína B em 5% e a proteína C reativa em 49%. A pressão arterial sistólica foi reduzida em 4% entre os participantes eutróficos e a pressão diastólica foi reduzida em 4% entre os participantes com excesso de peso. Não houve diminuição significativa das variáveis antropométricas. O consumo do suco de laranja vermelha aumentou em 907% a ingestão de vitamina C e 145% a ingestão de folato das mulheres, e 1130% de vitamina C e 123% de folato dos homens. A ingestão regular de suco de laranja vermelha apresentou... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: This study had as objective investigates the regular ingestion of the red orange juice over risk factors for the development of cardiovascular disease in adults residents in the cities of Araraquara (SP) and Matão (SP). The variety of red pulp orange is also known as Mombuca blood orange, and its color is due to the carotenoids, especially from beta-carotene and lycopene. The study included 19 men and 16 women, which received 750 mL/d of pasteurized red orange juice during 8 weeks. It was evaluated in all subjects: weigh, height, skin folds (triceps, biceps, subscapular and suprailiac), waist circumference and systolic and diastolic blood pressure. Biochemical parameters were accomplished for total cholesterol, HDL cholesterol, apolipoproteins A1 and B, C reactive protein, homocysteine, triglycerides and glucose. For hemodynamic assessment were observed systolic and diastolic blood pressure and dietary evaluation was estimated using 24h food record. All evaluations were accomplished before and after consumption of red orange juice. The results showed that the consumers of red orange juice decreased total cholesterol by 9%, LDLcholesterol by 11%, apo B by 5% and the C reactive protein by 49%. Systolic blood pressure was reduced 4% among eutrophic participants and the diastolic blood pressure reduced 4% among the pre-obese participants. There was no significant reduction on anthropometric variables. Consumption of red orange juice increased 10 folds the intake of vitamin C and double the intake of folate for all volunteers. Regular consumption of red orange juice has shown hypolipidemic and hypotensive properties, while both juices, from the red and yellow oranges, have shown antiinflammatory effects
Mestre
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Fok, Henry Wing Hang. "Ventricular-vascular coupling and central arterial pulse pressure." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/ventricularvascular-coupling-and-central-arterial-pulse-pressure(c9b79392-15e3-4c43-b940-10bb9cbe35f7).html.
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Central pulse pressure (cPP), a product of ventricular-arterial interaction, is an important determinant of cardiovascular outcomes in hypertension. The aim of this thesis is to advance the understanding of pulsatile haemodynamics and to explore mechanisms that may selectively reduce cPP. The conventional view is that cPP comprises a component determined by the direct interaction of myocardial contraction with the impedance of the proximal arterial tree (closely related to pulse wave velocity, PWV) and a component ‘augmentation pressure’ generated by pressure wave reflections from muscular conduit arteries. Surprisingly little is known regarding regulation of conduit artery tone despite its potential influence on cPP. In the first part of this thesis, muscular large arterial tone was examined using a human forearm blood flow model. Vasoactive substances were infused locally into the brachial artery and vasodilator responses of the radial artery, as a muscular conduit artery, and forearm resistance microvasculature were examined. Nitric oxide donors, in particular, glyceryl trinitrate (GTN) were found to have the most selective action on conduit arteries compared to other vasodilators. In the second part of the thesis, I examined whether the action of GTN to reduce augmentation pressure could be accounted for by this selective dilation of muscular arteries. GTN was given systemically and by intra-coronary infusion in patients undergoing cardiac catheterisation. Invasive aortic blood pressure and flow velocity were analysed in the time domain by wave intensity analysis. This allows separation of pressure into a forward component generated by myocardial contraction and a backward component generated by ‘reflection’ from the peripheral arterial tree. A surprising finding was that changes induced by GTN were mainly attributable to a reduction in forward rather than backward pressure waves. That this resulted from a change in myocardial contractility was confirmed by local intracoronary injection of GTN. The final part of the thesis examines the relative contribution of forward and backward pressure waves in hypertension. An elevated cPP in hypertensive compared to normotensive subjects was accounted for primarily by an increased forward pressure wave. That this was due to increased myocardial contractility was confirmed by examining whether the pattern of wave intensity seen in hypertension could be reproduced, in normotensive subjects, by the inotrope dobutamine (when compared to the vasoconstrictor norepinephrine used as a control). This thesis thus provides novel insight into a) regulation of conduit artery tone, and b) pulsatile haemodynamics, highlighting the contribution of left ventricular ejection characteristics in determining pressure augmentation and cPP.
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Wright, Gary Allan. "Prevalence of left ventricular hypertrophy in peripheral arterial disease and its relation to blood pressure." Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/d0f29144-6cbc-4838-bb86-315088fc024f.
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Objectives: To assess the prevalence of left ventricular hypertrophy (LVH) inpatients with newly diagnosed peripheral arterial disease (PAD). Methods: Consecutive patients referred for the first time for assessment of PAD with a history of intermittent claudication and ankle brachial pressure of index of ≤0.9 were recruited. All subjects underwent a full echocardiogram, office blood pressure and 24 hour ambulatory blood pressure monitoring. Results: Out of 350 subjects screened, left ventricular mass measurements were available on 227 (65%). The prevalence of LVH indexed to body surface area was 50%. In a multiple regression model the factors independently related to LVH were age, sex and history of diabetes. There was no relation between presence of LVH and 24 hour blood pressure. Conclusion: LVH is prevalent in patients with PAD and is not associated with 24 hour blood pressure.
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New, Karl James. "Exercise, arterial pressure control & systemic O₂ tension : implications for post exercise hypotension in hypertension." Thesis, University of South Wales, 2008. https://pure.southwales.ac.uk/en/studentthesis/exercise-arterial-pressure-control--systemic-o2-tension(b1d2c65b-00ef-429c-9afd-7c0452f13dbb).html.
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This thesis presents four studies investigating the phenomenon of post exercise hypotension in the human condition of pre (borderline)-hypertension. Study one investigated the effects of an acute bout of 30-minutes upright cycling on post exercise haemodynamics and compared the results to a non-exercise control condition. 9 pre-hypertensive males, mean arterial pressure (MAP) = 106 ± 5 mmHg (50 ± 10 yr), not on medication, were studied for 6 hours following 30-minutes of cycle exercise at 70% maximal oxygen consumption and following 30-minutes of seated rest. Results demonstrate that moderate intensity exercise exerts a modest fall (~6 mmHg) in arterial pressure with the hypotension sustained for 6-hours post exercise. The fall in arterial pressure equates to a significantly reduced after load when compared to both pre-exercise baseline and non-exercise control data taken at the same time of day. The arterial pressure responses transcended into a sustained reduction (20%) in systemic vascular resistance and reciprocal increase in vascular conductance for up to 2-hours post-exercise. Venous atrial natriuretic peptide (ANP) demonstrated an elevation (44%) following exercise and a significant decline (33%) in the post-exercise period mirroring the haemodynamic response. This research reveals that acute exercise is capable of sustained reductions in arterial pressure and vascular resistance beyond the usual labile fluctuations and that the octapeptide ANP may exert a modulatory influence over the post-exercise response. Increases in 02 tension beyond the physiological range induces complex effects on the circulatory system with a dominant vasoconstriction following hyperoxia. The purpose of study 2 was to assess the effects of hypoxic (16% 02) and hyperoxic (50% 62) exercise on subsequent haemodynamic control when compared with normoxia. 9 pre-hypertensive males, MAP = 106 ± 5 mmHg (50 ±10 yr), not on medication, performed 30-minutes of cycle exercise at 70% normoxic maximal oxygen consumption in hypoxia (16% O 2 ), hyperoxia (50% O 2) and normoxia(21% O2 ). Hyperoxic exercise blunted post-exercise haemodynamics by significantly attenuating the reductions (from normoxic baseline) in SVR (-45%, PO.05 vs. normoxic & hypoxic exercise immediately post-exercise) that persisted throughout 120-minutes recovery in normoxia (-35% vs. normoxic & hypoxic exercise, during recovery) and elicited a mildly hypertensive effect, with regards to MAP, whereas normoxic and hypoxic exercise elicited a hypotension compared to baseline (P < 0.05). Circulating ANP was decreased in the hyperoxic trial when compared with normoxic and hypoxic exercise [24.3 (13.4) v. 31.5 (16.3) and 29.6 (13.9) pg/ml, respectively; P < 0.05, pooled for state]. Changes in MAP were related to changes in ANP concentration only following hyperoxic exercise (r = 0.50, P < 0.01). These findings indicate that acute modest hyperoxia reflexively induces measurable physiological derangement partly explained by decreased circulating concentrations of ANP. Study three determined the role of free-radical mediated oxidative stress and redox regulation of circulating NO metabolism as a primary modulator of vascular tone following exercise in pre-hypertensive humans. Utilising the same cohort and exercise protocol as in study 1 venous blood was sampled from an antecubital vein. Plasma NO metabolites nitrate (NO" 3 ) and nitrite (NO"2 ) were determined fluorometrically, whilst S-Nitrosothiol (RSNO) concentrations were assayed by the Saville reaction Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH). Exercise led to a delayed increase in LOOH by 60- minutes post-exercise (0.69 ± 0.13 v. 0.86 ± 0.18 umol/1, respectively, P < 0.05), that remained elevated until termination of the trial 6-hours post-exercise. NO'a significantly fell below baseline by 120-minutes post-exercise (10.8 ± 3.3 v. 1.1 ±1.1 u.mol/1, respectively, P < 0.05), remaining attenuated for the remainder of the study.NO'i and RSNO were unmodified in the post-exercise period. In parallel to this finding the data also indicates a significant blunting in the hyperaemic response [SVR decreased from a 31% reduction immediately (within 1-minute) post-exercise to -13 and 8% at 60- and 120-minutes post-exercise, respectively, P < 0.05] and reversal of the hypotension (P < 0.05) over the same time frame as the augmented lipid peroxidation and attenuated circulating NO~3. These results indicate that augmented oxidative stress exerts a deleterious effect on post-exercise haemodynamics and implicates a potential redox regulation pathway of NO as being a mechanism by which free radical-induced oxidative stress blunts the degree of PEH in the recovery period. The final study investigated the potential role of a redox-mediated regulation of circulating NO bioavailability as a modulator of the augmented vasoconstriction following hyperoxic exercise. The same cohort and exercise protocol were employed as in study 2 and venous blood was assayed for NO"3 , NO'a, RSNO, LOOK, & lipid /water-soluble antioxidant concentrations. Similar adverse haemodynamic effects were noted following hyperoxic exercise as reported previously in study 2. RSNO showed a significant increase following hypoxic exercise only (P < Q.Q5, state x time, interaction), whereas NO~3, NO~2 and LOOH failed to differ between conditions (P > 0.05, main effect for state [02] and state x time, interaction effects). Ascorbic acid was mobilised in response to hyperoxic exercise when compared to normoxia (P < 0.05, main effect for state [O2] and state x time, interaction effects) being significantly elevated by 120-minutes post-exercise in hyperoxia compared to normoxia and hypoxia [75.1 (31) v. 39.5 (18.3) v. 46.7 (14.2) |amol/l, respectively, P < 0.05]. This data demonstrates an effective endogenous antioxidant response and argues against a redox regulation pathway of NO metabolism as a primary mediator of blunted vasodilatation in this scenario. This elucidates a more complex regulation of arterial tone, resulting from a metabolic pathway independent of NO in older subjects with pre-hypertension. This work demonstrates that (1) aerobic exercise exerts a hypotensive effect in humans with pre-hypertension, (2) ANP plays a part in the vasodilatation following exercise, (3) Free-radical mediated oxidative stress & subsequent modulation of NO metabolism exerts a deleterious influence on post-exercise haemodynamics (4) Acute hyperoxic exercise induces a sustained vasoconstriction that is mediated via circulating ANP concentration but not by redox regulation of NO metabolism.
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Sinha, Manish Darvesha. "Relation of pre-clinical arterial disease to blood pressure in children with chronic kidney disease." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/relation-of-preclinical-arterial-disease-to-blood-pressure-in-children-with-chronic-kidney-disease(e5a32de5-d862-442d-8505-5669ed54e54e).html.
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Childhood chronic kidney disease (CKD) is a devastating illness requiring life-long medical input, often progressing to end stage kidney disease (ESKD) requiring dialysis and renal transplantation. Despite an increasing number of children now surviving through childhood and early adulthood, heart disease remains one of the major causes of death in individuals with childhood-onset CKD as young adults and it is likely this relates to onset of pre-clinical cardiovascular disease developing during childhood. Arterial stiffening relates to the severity of CKD, being greatest in those with dialysis dependent CKD, and is thought to be driven, at least in part, by excess body weight, hypertension and metabolic changes associated with CKD but their contribution to arterial disease progression remains poorly understood. The relationship of blood pressure with arterial disease remains unclear in the paediatric literature. Previous studies performed in children pre-dialysis, those on dialysis and following kidney transplantation have measured pulse wave velocity (PWV) of the carotid-femoral pathway (i.e. mainly the aorta) and/or measures of carotid mechanics have been examined but these studies have been limited by lack of concurrent measures of carotid blood pressure (required to determine functional elasticity of the carotid artery). Furthermore, whilst the potential impact of age and blood pressure (BP) have been adjusted for, when comparing differences between children with and without CKD, this comparison has not been performed between age and blood pressure matched groups. The objectives of my thesis are to 1) to determine the use of an easy to perform, well tolerated technique to measure PWV in children. 2) to compare estimates of central aortic systolic pressure with that measured directly from catheter placed in the aortic root. 3) to determine typical estimates of systolic blood pressure amplification and 4) to determine the association of arterial function and structure with severity of childhood CKD and to examine the relation of these measures to blood pressure. 5) to design a controlled trial to evaluate effects of aggressive versus standard blood pressure control on cardiovascular target organ damage. My research findings report novel data relating to my project objectives. We compared two different techniques to measure PWV (volumetric and tonometric) and observed that the volumetric technique is easy to perform, well tolerated and reproducible when measurements are made by the same observer consecutively, but that the results are of the two techniques are not inter-changeable. My work for objective 2 and 3 measured central blood pressure at the aortic root at the time of arterial cannulation and confirmed that blood pressure measured in the arm differs from that close to the heart. We validated simple non-invasive methods to measure blood pressure in children and showed that peripheral systolic amplification is substantial, including those with and without hypertension and mild to advanced CKD, with a mean amplification of ~ 20 mmHg and thus may be relatively more important than in adults. In a cohort of children with and without CKD, we performed a comprehensive characterization of arterial biomechanics and observed that the changes in elastic properties of the carotid artery were related to increased blood pressure, and not to decreased glomerular filtration rate. Important limitations to this cross-sectional study include lack of knowledge of duration of both hypertension and CKD and lack of formal sample size calculation. Despite these limitations the results from my thesis suggest that blood pressure reduction may be an effective means to protect against arterial stiffening and needs to be evaluated using a controlled clinical trial. The design of such a trial is presented.
Books on the topic "Arterial pressure. eng"
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Rascher, Wolfgang. Treatment of hypertension in children. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0219_update_001.
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Management of hypertension is dependent on the underlying cause and the magnitude of the blood pressure abnormality. Healthy behavioural changes are the primary management tool for treating primary hypertension in adolescents and other cardiovascular risk factors and obesity. In children and adolescents with renal hypertension, high blood pressure requires pharmacological treatment. There is randomized controlled trial evidence to support a blood pressure target for those with proteinuria of not higher than the 50th centile for age. The use of angiotensin-converting enzyme inhibitors is safe in patients with proteinuria, and assumed to be equally beneficial. For those without proteinuria, less stringent targets may be acceptable. Often a combination of two or three drugs is required to lower arterial blood pressure to the target blood pressures. In children and adolescents at or near end-stage renal failure, fluid removal by dialysis may be necessary to control hypertension.
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Sainz, Jorge G., and Bradley P. Fuhrman. Basic Pediatric Hemodynamic Monitoring. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0005.
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Physiological monitoring using a variety of technological advances supplements, but does not replace, our ability to distinguish normal from abnormal physiology traditionally gleaned from physical examination. Pulse oximetry uses the wavelengths of saturated and unsaturated hemoglobin to estimate arterial oxygenation noninvasively. Similar technology included on vascular catheters provides estimation of central or mixed venous oxygenation and helps assess the adequacy of oxygen delivered to tissues. End-tidal carbon dioxide measurements contribute to the assessment of ventilation. Systemic arterial blood pressure and central venous pressure measurements help evaluate cardiac performance, including the impact of ventilatory support. Intra-abdominal pressure may increase as a result of intraluminal air or fluid, abnormal fluid collections within the peritoneal cavity, or abnormal masses. Increased pressure may impede venous return to the heart and compromise intra-abdominal organ perfusion. Pressure measurement guides related management decisions.
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Lee, Jae Myeong, and Michael R. Pinsky. Cardiovascular interactions in respiratory failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0087.
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Acute respiratory failure not only impairs gas exchange, but also stresses cardiovascular reserve by increasing the need for increased cardiac output (CO) to sustain O2 delivery in the face of hypoxaemia, increased O2 demand by the increased work of breathing and inefficient gas exchange, and increased right ventricular afterload due to lung collapse via hypoxic pulmonary vasoconstriction. Mechanical ventilation, though often reversing these processes by lung recruitment and improved arterial oxygenation, may also decrease CO by increasing right atrial pressure by either increasing intrathoracic pressure or lung over-distention by excess positive end-expiratory pressure or inadequate expiratory time causing acute cor pulmonale. Finally, spontaneous negative swings in intrathoracic pressure also increase venous return and impede left ventricular ejection thus increasing intrathoracic blood volume and often precipitating or worsening hydrostatic pulmonary oedema. Positive-pressure breathing has the opposite effects.
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Rascher, Wolfgang. The hypertensive child. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0218_update_001.
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Arterial hypertension is a well-recognized manifestation of various forms of renal disease both in adults and children. In the paediatric age group, standards for normal blood pressure are different from adults and have now been satisfactorily defined as have standards for measuring blood pressure. The epidemic of overweight and obesity in youth is increasing the prevalence of hypertension among children and adolescents. Measurement of blood pressure requires a technique specific for different age groups of the paediatric population, is more complex and requires particular expertise. Reference values in children requires adaptation to the age and size of the child and interpretation must be related to normative values specific for age, sex, and height. Evaluation for causes of secondary hypertension and for end-organ damage is basically similar in children as in adults. This chapter discusses measuring blood pressure, blood pressure standards, definition, classification, clinical presentation, and diagnostic approach to hypertension in children.
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Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.
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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
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Kipnis, Eric, and Benoit Vallet. Tissue perfusion monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0138.
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Resuscitation endpoints have shifted away from restoring normal values of routinely assessed haemodynamic parameters (central venous pressure, mean arterial pressure, cardiac output) towards optimizing parameters that reflect adequate tissue perfusion. Tissue perfusion-based endpoints have changed outcomes, particularly in sepsis. Tissue perfusion can be explored by monitoring the end result of perfusion, namely tissue oxygenation, metabolic markers, and tissue blood flow. Tissue oxygenation can be directly monitored locally through invasive electrodes or non-invasively using light absorbance (pulse oximetry (SpO2) or tissue (StO2)). Global oxygenation may be monitored in blood, either intermittently through blood gas analysis, or continuously with specialized catheters. Central venous saturation (ScvO2) indirectly assesses tissue oxygenation as the net balance between global O2 delivery and uptake, decreasing when delivery does not meet demand. Lactate, a by-product of anaerobic glycolysis, increases when oxygenation is inadequate, and can be measured either globally in blood, or locally in tissues by microdialysis. Likewise, CO2 (a by-product of cellular respiration) and PCO2 can be measured globally in blood or locally in accessible mucosal tissues (sublingual, gastric) by capnography or tonometry. Increasing PCO2 gradients, either tissue-to-arterial or venous-to-arterial, are due to inadequate perfusion. Metabolically, the oxidoreductive status of mitochondria can be assessed locally through NADH fluorescence, which increases in situations of inadequate oxygenation/perfusion. Finally, local tissue blood flow may be measured by laser-Doppler or visualized through intravital microscopic imaging. These perfusion/oxygenation resuscitation endpoints are increasingly used and studied in critical care.
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Especificaciones técnicas de la OMS para dispositivos automáticos de medición de la presión arterial no invasivos y con brazalete. Organización Panamericana de la Salud, 2020. http://dx.doi.org/10.37774/9789275323052.
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La hipertension es el principal factor de riesgo modificable de algunas enfermedades graves como las enfermedades cardiovasculares (accidentes cerebrovasculares y cardiopatías isquémicas), la preeclampsia y la eclampsia (una causa muy importante de muerte en las embarazadas, así como de retraso del crecimiento fetal y mortinatos) y la enfermedad renal crónica. A nivel mundial, más de mil millones de personas tienen hipertensión, y la prevalencia es mayor en los países de ingresos bajos y medianos. La medición exacta de la presión arterial es esencial para detectar y tratar adecuadamente a las personas con hipertensión, un trastorno que constituye un asesino silencioso que causa pocos síntomas. La falta de acceso a dispositivos de determinación de la presión arterial exactos y asequibles constituye un obstáculo importante para una atención médica adecuada, en particular en los entornos de recursos escasos. La medición manual está siendo reemplazada gradualmente por la medición automatizada debido a los problemas ambientales derivados del mercurio, la falta de calibración y las mediciones incorrectas de los dispositivos aneroides en la práctica clínica, así como por la exactitud uniforme superior que ofrecen los dispositivos automáticos validados. Sin embargo, con frecuencia existe cierta preocupación respecto a la exactitud de los dispositivos automatizados que no se han validado. Este documento actualiza la orientación de la OMS sobre dispositivos de medición de la presión arterial del 2005. También responde a la preocupación existente por la carencia de dispositivos exactos y de buena calidad, especialmente en los países de ingresos bajos y medianos mediante una consulta técnica y examen de expertos. Versión oficial en español de la obra original en inglés: WHO technical specifications for automated non-invasive blood pressure measuring devices with cuff. © World Health Organization, 2020 ISBN 978-92-4-000266-1 (print version)
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Galiè, Nazzareno, Alessandra Manes, and Massimiliano Palazzini. Pulmonary hypertension. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0065.
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Pulmonary hypertension is a haemodynamic and pathophysiological condition defined as an increase in the mean pulmonary arterial pressure of ≥25 mmHg at rest, as assessed by right heart catheterization. In fact, while transthoracic echocardiography may provide clues on the presence of pulmonary hypertension, the haemodynamic evaluation offers a more precise and comprehensive assessment. Pulmonary hypertension is heterogeneous from a pathophysiological point of view, and the diversity is reflected in the haemodynamic definitions. The different haemodynamic forms of pulmonary hypertension can be found in multiple clinical conditions which have been classified into six main groups and at least twenty-six subgroups. Each main clinical group shows specific pathological changes in the lung distal arteries, capillaries, and small veins. If we combine the haemodynamic and clinical heterogeneity, we understand the complexity of an accurate diagnosis in the individual patient which is crucial for the prognostic assessment and treatment strategy. In addition, the concomitant presence of different haemodynamic and clinical mechanisms cannot be excluded in individual cases (e.g. in patients with congestive heart failure and associated lung diseases). The presence of pulmonary hypertension, as defined above, is always an ominous prognostic sign, even if the severity may differ according to the haemodynamic changes and underlying clinical condition. The therapeutic approach also is markedly different, according to the clinical group, and symptomatic and haemodynamic severity. For these reasons, the four more frequent clinical groups are discussed individually, while the classifications are described in the Introduction section.
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Brallier, Jess W., and Jonathan S. Gal. Neuroprotection for Spine Surgery. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0020.
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Perioperative neurologic injury related to spine surgery, albeit rare, can result in devastating functional loss. As the number of spine operations has increased, so has the need for strategies designed to avoid and protect against such injury. This chapter reviews the common etiologies of neurologic deficits secondary to spine surgery and the factors that place patients at increased risk for developing these complications. The use of intraoperative neuromonitoring, including somatosensory evoked potentials (SSEPs), electromyography (EMG), and transcranial motor evoked potentials (TcMEPs), to detect surgical trespass of neuronal elements is also reviewed. The authors also summarize the role of physiologic parameter optimization, including mean arterial blood pressure and body temperature, and pharmacologic interventions, should an injury occur. Current practice guidelines for preventing and managing perioperative neurologic injury are described.
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Leaver, Susannah, and Timothy Evans. Hypoxaemia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0085.
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Hypoxaemia is a reduction in the partial pressure of oxygen in the blood below 8 kPa/60 mmHg. Hypoxaemia results from one, or several, or a combination of causes. Calculating the alveolar–arterial gradient can help to delineate the cause. Acute respiratory failure manifests in a number of ways, the most sensitive indicator being an increased respiratory rate. Diagnosis is dependent on a comprehensive history, examination in combination with appropriate blood tests, and imaging. Hypoxaemia is the final common pathway of a number of conditions and the exact cause may not be immediately apparent. Despite this, the same management principles apply. A trial of non-invasive ventilation can be used to support patients during respiratory failure who do not require immediate endotracheal intubation. However, it is recommended that this is instituted for a preset trial period (e.g. 1–2 hours) in an HDU/ICU setting where facilities for definitive airway management are available. Invasive ventilation aims to facilitate treatment of the underlying condition whilst minimizing side effects through lung protective ventilatory strategies.
Book chapters on the topic "Arterial pressure. eng"
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Morrell, Nicholas W. "Pulmonary hypertension." In Oxford Textbook of Medicine, edited by Jeremy Dwight, 3695–710. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0374.
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Symptoms of unexplained exertional breathlessness or symptoms out of proportion to coexistent heart or lung disease should alert the clinician to the possibility of pulmonary hypertension, and the condition should be actively sought in patients with known associated conditions, such as scleroderma, hypoxic lung disease, liver disease, or congenital heart disease. Heterozygous germ-line mutations in the gene encoding the bone morphogenetic protein type II receptor (BMPR2) are found in over 70% of families with pulmonary arterial hypertension. Pulmonary hypertension is defined as a mean pulmonary arterial pressure greater than 25 mm Hg at rest, and may be due to increased pulmonary vascular resistance (e.g. pulmonary arterial hypertension), increased transpulmonary blood flow (e.g. congenital heart disease), or increased pulmonary venous pressures (e.g. mitral stenosis). Exercise tolerance and survival in pulmonary hypertension is ultimately related to indices of right heart function, such as cardiac output.
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Munis, James R. "Starling’s Riddle of the Broken Heart." In Just Enough Physiology, 77–87. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199797790.003.0010.
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In 1897, Ernest Starling lectured on heart failure by inducing cardiac tamponade in an anesthetized dog. When the tamponade began to have an effect, the arterial pressure began to fall, but the venous pressures began to rise. In other words, heart failure didn't just decrease one type of pressure, it simultaneously increased another type of pressure. By the end of the experiment, all pressures had converged to the same value. The heart, like any pump, doesn't just raise fluid pressure on one side, it simultaneously lowers fluid pressure on the opposite side. The heart has a peculiar architecture that prefers a slightly filled resting state. Any smaller volume actually requires active contraction—it passively springs open during a part of diastole, suctioning blood into itself. Why then does heart failure cause capillary edema? We understand that the pressure in large veins will rise with heart failure, but capillary pressure is on the left side of the intersection of the curve and the Pms line. As such, capillary pressure should decrease with heart failure, and the tendency toward edema similarly should decrease.
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Munis, James R. "What Goes Around Comes Around—Venous Return." In Just Enough Physiology, 48–54. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199797790.003.0006.
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By its nature, circulatory physiology is also susceptible to circular reasoning because every part of an interconnected system is affected by, and affects, every other part. If we're not careful, we end up saying things like ‘venous return equals cardiac output’ when, in the steady state, that is true by definition and nothing new is gained. If we grant that right atrial pressure (PRA) is the ‘downstream’ pressure for venous return, then it follows that PRA should be inversely related to venous return (and therefore, to cardiac output). If we simply apply Ohm's law to the cardiovascular system, we forget that the mean arterial pressure not only contributes to venous return but also is sustained by venous return. If venous return fails for any other reason (unrelated to arterial pressure), so too will mean arterial pressure eventually fail.
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Simon, Chantal, Hazel Everitt, Françoise van Dorp, and Matt Burkes. "Cardiology and vascular disease." In Oxford Handbook of General Practice, 231–92. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199671038.003.0010.
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Symptoms and signs of CVD Examining the heart Examination of the arterial system Cardiac investigations Brief guide to common ECG changes Prevention of coronary heart disease Estimating cardiovascular risk Blood pressure measurement Hypertension Hyperlipidaemia Angina Drug treatment of angina After myocardial infarction Chronic heart failure...
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Magee, Patrick, and Mark Tooley. "Cardiac Output Measurement." In The Physics, Clinical Measurement and Equipment of Anaesthetic Practice for the FRCA. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199595150.003.0017.
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The pulmonary artery catheter was the mainstay of clinical cardiac output measurement for many years, but because of its relatively invasive nature and the lack of improvement of clinical outcome with its use, it is now seldom used in a modern clinical environment. Any perceived accuracy of the technique is now considered unnecessary in the face of the risks of its use, and with the introduction of newer non-invasive techniques. Nevertheless, it is worth describing, partly because of its historical interest, and partly because of the technologies involved. A catheter passed into the right atrium from an easily accessible central vein can be passed through the right ventricle and out into the pulmonary arterial tree while the vascular waveforms are visualised. Figure 13.1 shows the waveforms as they appear to the user. A small balloon at the tip of the catheter allows it to be flow directed and wedged in a pulmonary arterial vessel. At this point the pulsatile waveform is lost and the tip of the catheter is looking ahead, down the pulmonary arterial tree towards the left atrium, a system with a relatively low pressure drop from one end to the other, the flow in that vessel having been brought temporarily to a standstill. Thus the pulmonary artery occlusion pressure (PAOP) or pulmonary capillary wedge pressure (PCWP) can be considered a reasonably accurate representation of left atrial pressure or left ventricular filling pressure. This assumes that there is no pulmonary vascular disease, such as pulmonary hypertension, or mitral valve disease, in which case PAOP would not be an accurate representation of left atrial pressure. If the catheter is placed in the apical region of the pulmonary vascular tree, the excess of the alveolar pressure in inspiration over pulmonary capillary pressure becomes significant, and the latter is a less accurate reflection of left atrial pressure. The balloon should not be over-inflated for fear of rupturing the pulmonary artery, and this is one of its perceived risks that has led to less usage. Once the measurement has been made, the balloon should be deflated so that the pulmonary arterial waveform is once again visible, if necessary withdrawing the catheter a bit to achieve this; failure to do so would result in regional lack of perfusion and may result in ischaemia.
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Palazzini, Massimiliano, Nazzareno Galiè, and Alessandra Manes. "Pulmonary hypertension." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 839–48. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0063.
Full textAbstract:
Pulmonary hypertension is a haemodynamic and pathophysiological condition defined as an increase in the mean pulmonary arterial pressure of ?25 mmHg at rest, as assessed by right heart catheterization. Recently, a new definition has been proposed as mean pulmonary arterial pressure >20 mmHg combined with pulmonary vascular resistance ? 3 Wood units. While transthoracic echocardiography may provide clues on the presence of pulmonary hypertension, the haemodynamic evaluation offers a more precise and comprehensive assessment. Pulmonary hypertension is heterogeneous from a pathophysiological point of view, and the diversity is reflected in the haemodynamic definitions. The different haemodynamic and clinical forms of pulmonary hypertension can be found in multiple clinical conditions which have been classified into five main groups and at least twenty-six subgroups. Each main clinical group shows specific pathological changes in the lung distal arteries, capillaries, and small veins. If we combine the haemodynamic and clinical heterogeneity, we understand the complexity of an accurate diagnosis in the individual patient which is crucial for the prognostic assessment and treatment strategy. In addition, the concomitant presence of different haemodynamic and clinical mechanisms cannot be excluded in individual cases (e.g. in patients with congestive heart failure and associated lung diseases). The presence of pulmonary hypertension, as defined above, is always an ominous prognostic sign, even if the severity may differ according to the haemodynamic changes and underlying clinical condition. The therapeutic approach also is markedly different, according to the clinical group, and symptomatic and haemodynamic severity. For these reasons, the four more frequent clinical groups are discussed individually, while the classifications are described in the Introduction section.
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Farne, Hugo, Edward Norris-Cervetto, and James Warbrick-Smith. "Leg ulcer." In Oxford Cases in Medicine and Surgery. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780198716228.003.0035.
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Venous ulcers account for by far the majority (about 70%), with mixed arterial/venous (about 10%) and arterial (about 10%) most of the remainder. Pressure ulcers have become increasingly common because of the increase in elderly, frail, and relatively immobile patients. The other causes are relatively rare with the exception of neuropathic ulcers in patients with diabetes mellitus. Note that many leg ulcers may have a multifactorial aetiology, i.e. they may involve more than one of the pathologies listed in Figure 29.1. The first thing is to ask about the ulcer. You should consider: • Is the ulcer painful? ■ Venous ulcers are caused by venous stasis in the leg and are thus less painful when elevated and drained of blood. However, only about 30% of venous ulcers are painful. ■ Arterial (atherosclerotic) ulcers are caused by ischaemia to the leg and are thus more painful when elevated and drained of blood. Patients often say the ulcers are painful enough to wake them up at night and that they obtain relief by lowering their leg over the side of the bed. ■ Neuropathic ulcers are caused by loss of sensation (which predisposes to constant trauma) and are thus not painful. ■ Pressure ulcers are caused by, as the name suggests, prolonged pressure on the affected site. They tend to be exquisitely tender but not necessarily painful if no pressure is being applied. • How long has the ulcer been there? ■ Venous ulcers are less painful and can therefore present late. They often have a long and recurring history. ■ Arterial ulcers tend to present relatively early because of pain. They often occur secondary to trivial trauma. ■ Neuropathic ulcers are associated with a loss of sensation and thus often present late. ■ Pressure ulcers can develop surprisingly rapidly (e.g. days in immobile patients if they are not turned regularly during their admission, even hours in patients who suffer a long lie following a fall), but can have a more indolent course depending on how much pressure is put on for how long. Thus the time course is not especially helpful. ■ A long history should arouse suspicion of a Marjolin ulcer, which only occurs in long-standing ulcers.
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Andriessen, Peter. "Autonomic Cardiovascular Regulation in the Newborn." In Neonatal Monitoring Technologies, 201–21. IGI Global, 2012. http://dx.doi.org/10.4018/978-1-4666-0975-4.ch009.
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This paper reviews the baroreflex mediated heart rate response in human infants with a focus on data acquisition, signal processing and autonomic cardiovascular modeling. Baroreflex mediated heart rate response is frequently used as an estimate of autonomic cardiovascular regulation. Baroreflex mediated heart rate response may be viewed in terms of a negative-feedback system. To study fluctuations in this feedback system, continuous registration of ECG and blood pressure waveforms are required. From these waveforms, time series of R-R interval and blood pressure values are derived. This paper focus on spontaneous baroreflex sensitivity (e.g., R-R interval change per unit of arterial blood pressure change, ms/mmHg) calculated from cross-spectral analysis of spontaneous occurring changes in R-R interval and blood pressure. Despite different methodology (sequence method; transfer function analysis; head-up tilt) there is fairly good agreement of spontaneous baroreflex sensitivity values during homeostasis. Preterm infants and term newborns have values of 2-4 and 10-15 ms/mmHg, respectively. These values are much lower than found in adults, approximately 25 ms/mmHg. The clinical relevance of a limited baroreflex function may be that acute perturbations of the cardiovascular system are poorly counteracted and may result in poor cerebral perfusion.
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"Practical procedures." In Oxford Handbook for Medical School, edited by Kapil Sugand, Miriam Berry, Imran Yusuf, Aisha Janjua, Chris Bird, David Metcalfe, Harveer Dev, et al., 821–38. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199681907.003.0045.
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This chapter gives clear guidance on practical procedures which most medical students would be expected to be competent at by the end of their training. The beginning of the chapter advises on the importance of strict hand hygiene in protecting patients from unnecessary infection. The chapter also explains how to measure blood pressure manually. Advice is given on how to place a nasogastric tube and how to place a urethral catheter, with radiographs and illustrations to help clarify anatomy and ensure against false passage. Clear advice is given on how to set up for and perform both venepuncture and intravenous cannulation, with advice on common anatomical sites for these procedures, contraindications, and first aid for needle-stick injuries. For emergencies, interosseous access is also discussed. How to obtain an arterial blood gas is explained, including the Allen test to ensure adequate ulnar arterial blood flow if sampling from the radial artery. The chapter also explains how to measure the ankle–brachial pressure index and basic plastering. Adequate supervision by senior staff is emphasized throughout.
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Emmett, Stevan R., Nicola Hill, and Federico Dajas-Bailador. "Renal medicine." In Clinical Pharmacology for Prescribing. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780199694938.003.0013.
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The kidneys are of fundamental importance in the regulation of fluid and electrolytes, maintaining permissive extracellular fluid composition (salts and water), pH, and volume, while also mediating the removal of waste products. Based on the anatomy of the nephron, three main processes occur in order to deliver this balance: glomerular filtration, tubular secretion, and tubular resorption. Drugs can act at different sites within this system, so that functional equilibrium can be restored in various disease states (e.g. hypertension, heart failure, liver failure, nephrotic syndrome). CKD is a long- term condition that lasts more than 3 months and affects the function of both kidneys. It results from any pathology that reduces renal functional capacity and produces a decrease in GFR to less than 60 mL/ min/ 1.73 m<sup>2</sup>. Prevalence within the UK is high, particularly in the elderly and affects 6– 8% of the population. The most common cause of CKD is idiopathic (unknown, usually with small kidneys), then diabetes mellitus. In both, glomerular damage and mesangial injury (causing metabolic and haemodynamic effects) occur. Mild- moderate essential hypertension does not cause CKD. Knowledge of the functional anatomy of the proximal tubule and loop of Henle is essential in understanding therapeutic targets and treatment of pathologies, as each region and transporter system has a key role. In brief, the journey of solutes from the blood to the production of urine occurs at five main anatomical sites— the glomerulus, the proximal tubule, the loop of Henle, the distal tubule (proximal part and distal part), and the collecting ducts (Figures 5.1 and 5.2). The glomerulus is a network of capillaries (like a ball of string), which merge with the nephron via Bowman’s capsule. It is the first site of filtration and the place where solutes, toxins, and small proteins are removed from the wider circulatory system, after delivery by the renal arteries (via an afferent arteriole). Blood and larger proteins remain in the arteriole and leave via an efferent branch, while the filtrate enters the proximal convoluted tubule. The afferent:efferent system ensures that a constant filtration pressure is maintained irrespective of variations in arterial pressure. The capillary bed is very large, so that permeability and filtration rates are high. A normal glomerular filtration rate (GFR) i.e. 90– 120 mL/ min/ 1.73 m<sup>2</sup>, depends on hydrostatic pressure, the colloid osmotic pressure and hydraulic per¬meability.
Conference papers on the topic "Arterial pressure. eng"
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Paviglianiti, Annunziata, Vincenzo Randazzo, Eros Pasero, and Alberto Vallan. "Noninvasive Arterial Blood Pressure Estimation using ABPNet and VITAL-ECG." In 2020 IEEE International Instrumentation and Measurement Technology Conference (I2MTC). IEEE, 2020. http://dx.doi.org/10.1109/i2mtc43012.2020.9129361.
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CONTE, E., and A. FEDERICI. "CHAOTIC PARAMETERS IN TIME SERIES OF ECG, RESPIRATORY MOVEMENTS AND ARTERIAL PRESSURE." In Modelling Biomedical Signals. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812778055_0004.
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Pachauri, Awadhesh, and Manabendra Bhuyan. "Synthesis of ECG from arterial blood pressure and central venous pressure signals using Artificial Neural Network." In 2014 Recent Advances and Innovations in Engineering (ICRAIE). IEEE, 2014. http://dx.doi.org/10.1109/icraie.2014.6909209.
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van Geel, M. H. A., C. G. Giannopapa, B. J. van der Linden, and J. M. B. Kroot. "Development of a Blood Flow Model Including Hypergravity and Validation Against an Analytical Model." In ASME 2010 Pressure Vessels and Piping Division/K-PVP Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/pvp2010-26149.
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Fluid structure interaction (FSI) appears in many areas of engineering, e.g. biomechanics, aerospace, medicine and other areas and is often motivated by the need to understand arterial blood flow. FSI plays a crucial role and cannot be neglected when the deformation of a solid boundary affects the fluid behavior and vice versa. This interaction plays an important role in the wave propagation in liquid filled flexible vessels. Additionally, the effect of hyper gravity under certain circumstances should be taken into account, since such exposure can cause alterations in the wave propagation underexposed. Typical examples in which hyper gravity occurs are rollercoaster rides and aircraft or spacecraft flights. This paper presents the development of an arterial blood flow model including hyper gravity. This model has been developed using the finite element method along with the ALE method. This method is used to couple the fluid and structure. In this paper straight and tapered aortic analogues are included. The obtained computational data for the pressure is compared with analytical data available.
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Qiao, Aike, and Teruo Matsuzawa. "Hemodynamics of End-to-End Femoral Bypass Graft." In ASME/JSME 2004 Pressure Vessels and Piping Conference. ASMEDC, 2004. http://dx.doi.org/10.1115/pvp2004-3125.
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In the conventional femoral bypassing operation, side-to-end (STE) configuration at the proximal anastomosis and end-to-side (ETS) configuration at the distal anastomosis are usually employed. With these configurations, blood flow from the bypass graft at the distal anastomosis strongly strikes on the floor of the host artery opposite the anastomosis. This will result in the violent variations of hemodynamics in the vicinity of distal anastomosis, and further bring about anastomotic intimal hyperplasia (IH) and restenosis. Consequently, the effectiveness of bypassing surgery is compromised in the medium and long term by the development of these pathological changes. It is widely accepted that hemodynamics is close correlated to the geometry configuration of femoral bypass graft. It is verified that flow field at the distal junction has more influences on the pathogenesis and its aftereffects are more critical because the development of IH and restenosis is prone to occur in that region and endangers the patency of subsequent arteries. Nonuniform hemodynamics, characterized by nonuniform Wall Shear Stress (WSS) and large sustained Wall Shear Stress Gradients (WSSG), is also commonly considered as one of the most important causes among the numerous complex physiological and biomechanical factors. Purpose of the present study is to investigate an alternative geometry configuration to improve the hemodynamics at the vicinity of distal anastomosis and increase the medium and long term patency rate of bypass graft surgery. According to the clinical observation, the stenosed host artery may become fully stenosed after bypassing surgery and the bypass graft is the only way to restore normal blood flow to ischemic limbs. The authors presented a modified bypassing configuration with an end-to-end (ETE) conjunction at the distal anastomosis. In this new model, the proximal graft is arc-shaped with STE junction and the distal graft is sinusoid-shaped with ETE junction. The bypass graft is of the same diameter of d = 8mm as the host femoral artery, so the graft can be connected with the femoral artery smoothly at the distal junction. The polytetrafluoroethylene (PTFE) is employed as the graft material. The blood is assumed to be an isotropic, homogeneous, incompressible, Newtonian continuum having a constant density and viscosity. The vessel walls are assumed to be rigid and impermeable. The blood flow is assumed to be physiologically pulsatile laminar flow. The mean Reynolds number is Rem = 204.7, Womersley number is α = 6.14. The boundary conditions include: the physiologically pulsatile entrance velocities at the inlet section, the no-slip boundary condition on the wall, the symmetric condition in the centerline plane of femoral and graft, and the outlet pressure condition with a reference pressure P = 0 at the exit section. Three-dimensional idealized femoral bypass graft model is developed and discretized. The blood flow in the proposed model is simulated with computational fluid dynamics (CFD) method using the finite element analysis. The temporal and spatial distributions of hemodynamics such as flow patterns and WSS in the vicinity of distal anastomosis during the cardiac cycle were analyzed. Especially, the emphasis here was on the analysis of WSS, the temporal and spatial WSSG and the Oscillating Shear Index (OSI). The simulation results indicated that: (1) the ETE model is featured with small secondary flow; (2) WSS at the distal anastomosis is uniform, WSSG is small, and OSI of the ETE model has not much changes compared with ETS graft. The present study showed that the femoral bypassing configuration with ETE bypass graft was of more favorable hemodynamics, and it could consequently improve the flow conditions and decrease the probability of IH and restenosis. With the consideration of that numerical simulation was proved to be of great help and guidance meaning for the biofluidmechanics research and the biomedical engineering, the results of the present study can be applied to medical device design and clinical treatment planning in addition to the application of computational methods to cardiovascular disease research.
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Bijnens, Nathalie, Bart Beulen, Peter Brands, Marcel Rutten, and Frans van de Vosse. "Towards Non-Invasive Pressure Assessment." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19214.
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In clinical practice, ultrasound is frequently applied to non-invasively assess blood velocity, blood volume flow and blood vessel wall properties such as vessel wall thickness and vessel diameter waveforms. To convert these properties into relevant biomechanical properties that are related to cardiovascular disease (CVD), such as elastic modulus and compliance of the vessel wall, local pressure has to be assessed simultaneously with vessel wall thickness and vessel diameter waveforms. Additionally, accurate estimates of vascular impedance (transfer function between pressure and blood flow) can be a valuable tool for the estimation of the condition of the vessel, e.g., to diagnose stenosis. Studies of arterial impedance in humans, however, are hampered by the lack of reliable non-invasive techniques to simultaneously record pressure and flow locally as a function of time. Local pressure assessment together with flow has great potential for improving the ability to diagnose and monitor CVD.
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Lopez, Alexandra, Yury Jimenez, Raul Bareno, Brayan Balamba, and Juan Sacristan. "E-Health System for The Monitoring, Transmission and Storage of The Arterial Pressure of Chronic-Hypertensive Patients." In 2019 Congreso Internacional de Innovación y Tendencias en Ingenieria (CONIITI ). IEEE, 2019. http://dx.doi.org/10.1109/coniiti48476.2019.8960803.
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Zong, Wei. "Reduction of false critical ECG alarms using waveform features of arterial blood pressure and/or photoplethysmogram signals." In 2015 Computing in Cardiology Conference (CinC). IEEE, 2015. http://dx.doi.org/10.1109/cic.2015.7408643.
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Manorama, Abinand, and Tamara Reid Bush. "Skin Perfusion, Arterial and Venous Blood Flow, and Soft Tissue Thickness in Relation to Pressure Ulcers." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14496.
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Pressure ulcers have been a concern in healthcare settings, with more than 50% of bedridden or wheelchair-bound patients being affected [1]. Pressure ulcers typically occur on a region of the body that experiences forces from an external structure (e.g. bed, wheelchair). Researchers believe that such forces cause a decrease in blood flow, which results in tissue necrosis, causing pressure ulcers [2].
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Verma, Ajay K., John Zanetti, Reza Fazel-Rezai, and Kouhyar Tavakolian. "Pulse Transit Time Derivation Using Xiphoidal and Carotid Seismocardiograms." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3444.
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Blood pressure is an indicator of a cardiovascular functioning and could provide early symptoms of cardiovascular system impairment. Blood pressure measurement using catheterization technique is considered the gold standard for blood pressure measurement [1]. However, due its invasive nature and complexity, non-invasive techniques of blood pressure estimation such as auscultation, oscillometry, and volume clamping have gained wide popularity [1]. While these non-invasive cuff based methodologies provide a good estimate of blood pressure, they are limited by their inability to provide a continuous estimate of blood pressure [1–2]. Continuous blood pressure estimate is critical for monitoring cardiovascular diseases such as hypertension and heart failure. Pulse transit time (PTT) is a time taken by a pulse wave to travel between a proximal and distal arterial site [3]. The speed at which pulse wave travels in the artery has been found to be proportional to blood pressure [1, 3]. A rise in blood pressure would cause blood vessels to increase in diameter resulting in a stiffer arterial wall and shorter PTT [1–3]. To avail such relationship with blood pressure, PTT has been extensively used as a marker of arterial elasticity and a non-invasive surrogate for arterial blood pressure estimation. Typically, a combination of electrocardiogram (ECG) and photoplethysmogram (PPG) or arterial blood pressure (ABP) signal is used for the purpose of blood pressure estimation [3], where the proximal and distal timing of PTT (also referred as pulse arrival time, PAT) is marked by R peak of ECG and a foot/peak of a PPG, respectively. In the literature, it has been shown that PAT derived using ECG-PPG combination infers an inaccurate estimate of blood pressure due to the inclusion of isovolumetric contraction period [1–3, 4]. Seismocardiogram (SCG) is a recording of chest acceleration due to heart movement, from which the opening and closing of the aortic valve can be obtained [5]. There is a distinct point on the dorso-ventral SCG signal that marks the opening of the aortic valve (annotated as AO). In the literature, AO has been proposed for timing the onset of the proximal pulse of the wave [6–8]. A combination of AO as a proximal pulse and PPG as a distal pulse has been used to derive pulse transit time and is shown to be correlated with blood pressure [7]. Ballistocardiogram (BCG) which is a measure of recoil forces of a human body in response to pumping of blood in blood vessels has also been explored as an alternative to ECG for timing proximal pulse [5, 9]. Use of SCG or BCG for timing the proximal point of a pulse can overcome the limitation of ECG-based PTT computation [6–7, 9]. However, a limitation of current blood pressure estimation systems is the requirement of two morphologically different signals, one for annotating the proximal (ECG, SCG, BCG) and other for annotating the distal (PPG, ABP) timing of a pulse wave. In the current research, we introduce a methodology to derive PTT from seismocardiograms alone. Two accelerometers were used for such purpose, one was placed on the xiphoid process of the sternum (marks proximal timing) and the other one was placed on the external carotid artery (marks distal timing). PTT was derived as a time taken by a pulse wave to travel between AO of both the xiphoidal and carotid SCG.