Gotowe bibliografie tematyczne / De novo acute respiratory failure

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Gotowa bibliografia na temat „De novo acute respiratory failure”

Autor: Grafiati

Data publikacji: 21 września 2024

Data aktualizacji: 7 lipca 2025

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Artykuły w czasopismach na temat "De novo acute respiratory failure"

Petitjeans, Fabrice, and Luc Quintin. "Noninvasive Failure in De Novo Acute Hypoxemic Respiratory Failure." Critical Care Medicine 44, no. 11 (2016): e1153-e1154. http://dx.doi.org/10.1097/ccm.0000000000001967.

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Carteaux, Guillaume, Teresa Millán-Guilarte, Nicolas De Prost, et al. "Failure of Noninvasive Ventilation for De Novo Acute Hypoxemic Respiratory Failure." Critical Care Medicine 44, no. 2 (2016): 282–90. http://dx.doi.org/10.1097/ccm.0000000000001379.

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García-de-Acilu, Marina, Bhakti K. Patel, and Oriol Roca. "Noninvasive approach for de novo acute hypoxemic respiratory failure." Current Opinion in Critical Care 25, no. 1 (2019): 54–62. http://dx.doi.org/10.1097/mcc.0000000000000570.

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Costa, Bárbara. "Ventilação Não-Invasiva na Falência Respiratória Aguda." Medicina Interna 28, no. 2 (2021): 133–39. http://dx.doi.org/10.24950/o/320/20/2/2021.

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Introdução: A ventilação não invasiva (VNI) é uma opção válida, ainda que não consensual, no tratamento de doentes com falência respiratória aguda. O presente artigo tem o objetivo de identificar fatores preditores de resposta à VNI neste grupo de doentes. Métodos: Estudo retrospectivo longitudinal que incluiu todos os doentes admitidos numa unidade de cuidados intensivos nos anos 2016 e 2017, nos quais a VNI foi utilizada no decurso de falência respiratória aguda de novo (PaO2/ FiO2 < 200). Foram incluídos doentes com pneumonia adquirida na comunidade (PAC) e síndrome da dificuldade respiratória aguda (SDRA) e comparados doentes com resposta à VNI com os não respondedores. Resultados: Entre 2016 e 2017, 83 doentes com falência respiratória aguda de novo foram tratados com VNI. Destes, 50 (60%) foram tratados com sucesso. A causa mais comum de falência respiratória foi a PAC, que registou valores de resposta à VNI de 70%. Doentes respondedores à terapêutica de ventilação não invasiva apresentaram scores de gravidade (APACHE 2; SAPS 2; SOFA) inferiores à admissão (17,5; 37,5; 6 vs 22; 48; 9, p=0,014, p<0,01 e p<0,01, respetivamente). Os não respondedores apresentaram valores significativamente inferiores de pH arterial (7,35 vs 7,42, p<0,01), rácio PaO2/FiO2 (118 vs 145, p=0,03), e valores significativamente superiores de lactato sérico (2,2 vs 1,46, p<0,01) assim como maior necessidade de suporte vasopressor (51,5% vs 30%, p=0,04). No que diz respeito a dados gasimétricos após início de VNI, o rácio PaO2/FiO2 registou um aumento superior e estatisticamente significativo no grupo de doentes com resposta à VNI (+53, p<0,01 vs +14, p=0,09). Conclusão: A VNI foi eficaz como estratégia ventilatória em 60% dos doentes com falência respiratória aguda. Os doentes que aparentam ter maior probabilidade de resposta à introdução da VNI são: doentes com PAC, com ou sem SDRA moderado (em detrimento do SDRA severo), doentes sem acidemia respiratória e doentes sem hiperlactacidemia e/ou necessidade de suporte vasopressor. A melhoria do ratio PaO2/FiO2 após as primeiras duas horas de VNI parece ser um bom preditor de sucesso.

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Park, Sunghoon. "Treatment of acute respiratory failure: noninvasive mechanical ventilation." Journal of the Korean Medical Association 65, no. 3 (2022): 144–50. http://dx.doi.org/10.5124/jkma.2022.65.3.144.

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Background: Noninvasive ventilation (NIV) has been an important strategy to support patients with respiratory failure, while preventing complications assorted with invasive mechanical ventilation. Physicians need to be aware of the various roles of NIV and the challenges encountered in clinical practice.Current Concepts: Traditionally, the application of NIV has been well-known to be associated with reduced mortality in patients with chronic obstructive pulmonary disease (COPD) or acute pulmonary edema and those suffering from acute respiratory failure. However, despite some positive results of NIV treatment in patients with de novo hypoxemic respiratory failure such as acute pneumonia or acute respiratory distress syndrome, NIV failure (or delayed intubation) can have deleterious effects on patients outcomes. Besides, the aggravation of lung injury should also be taken into consideration when applied to patients exhibiting high respiratory drive. Nonetheless, NIV has potential for wide applications in various clinical situations such as facilitation of ventilator weaning, post-operative respiratory failure, or palliative treatment.Discussion and Conclusion: In addition to the strong evidence in patients with acute respiratory failure due to COPD or acute pulmonary edema, the NIV treatment can be potentially used for various clinical conditions. However, compared to European countries, the prevalence of NIV use continues to remain lower in South Korea. Nevertheless, when applied in appropriately selected patients in a timely manner, NIV treatment can be associated with improved patient outcomes.

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Zayed, Yazan, Mahmoud Barbarawi, Babikir Kheiri, et al. "Initial Noninvasive Oxygenation Strategies in Subjects With De Novo Acute Hypoxemic Respiratory Failure." Respiratory Care 64, no. 11 (2019): 1433–44. http://dx.doi.org/10.4187/respcare.06981.

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Spicuzza, Lucia, and Matteo Schisano. "High-flow nasal cannula oxygen therapy as an emerging option for respiratory failure: the present and the future." Therapeutic Advances in Chronic Disease 11 (January 2020): 204062232092010. http://dx.doi.org/10.1177/2040622320920106.

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Conventional oxygen therapy (COT) and noninvasive ventilation (NIV) have been considered for decades as frontline treatment for acute or chronic respiratory failure. However, COT can be insufficient in severe hypoxaemia whereas NIV, although highly effective, is poorly tolerated by patients and its use requires a specific expertise. High-flow nasal cannula (HFNC) is an emerging technique, designed to provide oxygen at high flows with an optimal degree of heat and humidification, which is well tolerated and easy to use in all clinical settings. Physiologically, HFNC reduces the anatomical dead space and improves carbon dioxide wash-out, reduces the work of breathing, and generates a positive end-expiratory pressure and a constant fraction of inspired oxygen. Clinically, HFNC effectively reduces dyspnoea and improves oxygenation in respiratory failure from a variety of aetiologies, thus avoiding escalation to more invasive supports. In recent years it has been adopted to treat de novo hypoxaemic respiratory failure, exacerbation of chronic obstructive pulmonary disease (COPD), postintubation hypoxaemia and used for palliative respiratory care. While the use of HFNC in acute respiratory failure is now routine as an alternative to COT and sometimes NIV, new potential applications in patients with chronic respiratory diseases (e.g. domiciliary treatment of patients with stable COPD), are currently under evaluation and will become a topic of great interest in the coming years.

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Lindstedt, Sandra, Edgar Grins, Hillevi Larsson, et al. "Lung transplant after 6 months on ECMO support for SARS-CoV-2-induced ARDS complicated by severe antibody-mediated rejection." BMJ Open Respiratory Research 8, no. 1 (2021): e001036. http://dx.doi.org/10.1136/bmjresp-2021-001036.

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There have been a few reports of successful lung transplantation (LTx) in patients with SARS-CoV-2-induced acute respiratory distress syndrome (ARDS); however, all reports were with rather short follow-up. Here we present a 62-year-old man without prior lung diseases. Following SARS-CoV-2-induced ARDS and 6 months of extracorporeal membrane oxygenation, he underwent LTx. 3 months post-transplantation he developed acute hypoxia requiring emergency intubation. Chest imaging showed acute rejection, and de novo DQ8-DSA was discovered. He was treated with a high dose of corticosteroids and plasmapheresis and was extubated 4 days later, yet the de novo DQ8-DSA remained. After sessions of plasmapheresis and rituximab, the levels of de novo DQ8-DSA remained unchanged. Nine months post-transplantation the patient died of respiratory failure. We herein discuss the decision to transplant, the transplantation itself and the postoperative course with severe antibody-mediated rejection. In addition, we evaluated the histological changes of the explanted lungs and compared these with end-stage idiopathic pulmonary fibrosis tissue, where both similarities and differences are seen. With the current case experience, one might consider close monitoring regarding DSA, and gives further support that LTx should only be considered for very carefully selected patients.

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Coudroy, Rémi, Jean-Pierre Frat, Stephan Ehrmann, et al. "High-flow nasal oxygen therapy alone or with non-invasive ventilation in immunocompromised patients admitted to ICU for acute hypoxemic respiratory failure: the randomised multicentre controlled FLORALI-IM protocol." BMJ Open 9, no. 8 (2019): e029798. http://dx.doi.org/10.1136/bmjopen-2019-029798.

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IntroductionNon-invasive ventilation (NIV) is recommended as first-line therapy in respiratory failure of critically ill immunocompromised patients as it can decrease intubation and mortality rates as compared with standard oxygen. However, its recommendation is only conditional. Indeed, the use of NIV in this setting has been challenged recently based on results of trials finding similar outcomes with or without NIV or even deleterious effects of NIV. To date, NIV has been compared with standard oxygen but not to high-flow nasal oxygen therapy (HFOT) in immunocompromised patients. Several studies have found lower mortality rates using HFOT alone than when using HFOT with NIV sessions in patients with de novo respiratory failure, and even in immunocompromised patients. We are hypothesising that HFOT alone is more effective than HFOT with NIV sessions and reduces mortality of immunocompromised patients with acute hypoxemic respiratory failure.Methods and analysisThis study is an investigator-initiated, multicentre randomised controlled trial comparing HFOT alone or with NIV in immunocompromised patients admitted to intensive care unit (ICU) for severe acute hypoxemic respiratory failure. Around 280 patients will be randomised with a 1:1 ratio in two groups. The primary outcome is the mortality rate at day 28 after inclusion. Secondary outcomes include the rate of intubation in each group, length of ICU and hospital stay and mortality up to day 180.Ethics and disseminationThe study has been approved by the ethics committee and patients will be included after informed consent. The results will be submitted for publication in peer-reviewed journals.Trial registration numberNCT02978300

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Boulos, Peter K., Scott V. Freeman, Timothy D. Henry, Ehtisham Mahmud, and John C. Messenger. "Interaction of COVID-19 With Common Cardiovascular Disorders." Circulation Research 132, no. 10 (2023): 1259–71. http://dx.doi.org/10.1161/circresaha.122.321952.

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The onset and widespread dissemination of the severe acute respiratory syndrome coronavirus-2 in late 2019 impacted the world in a way not seen since the 1918 H1N1 pandemic, colloquially known as the Spanish Flu. Much like the Spanish Flu, which was observed to disproportionately impact young adults, it became clear in the early days of the coronavirus disease 2019 (COVID-19) pandemic that certain groups appeared to be at higher risk for severe illness once infected. One such group that immediately came to the forefront and garnered international attention was patients with preexisting cardiovascular disease. Here, we examine the available literature describing the interaction of COVID-19 with a myriad of cardiovascular conditions and diseases, paying particular attention to patients diagnosed with arrythmias, heart failure, and coronary artery disease. We further discuss the association of acute COVID-19 with de novo cardiovascular disease, including myocardial infarction due to coronary thrombosis, myocarditis, and new onset arrhythmias. We will evaluate various biochemical theories to explain these findings, including possible mechanisms of direct myocardial injury caused by the severe acute respiratory syndrome coronavirus-2 virus at the cellular level. Finally, we will discuss the strategies employed by numerous groups and governing bodies within the cardiovascular disease community to address the unprecedented challenges posed to the care of our most vulnerable patients, including heart transplant recipients, end-stage heart failure patients, and patients suffering from acute coronary syndromes, during the early days and height of the COVID-19 pandemic.

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Rozprawy doktorskie na temat "De novo acute respiratory failure"

Berrube, Élise. "Patient self-inflicted lung injury et ventilator induced lung injury : De l'insuffisance respiratoire aiguë de novo à l'exacerbation aiguë de pneumopathie intersititielle diffuse." Electronic Thesis or Diss., Normandie, 2024. http://www.theses.fr/2024NORMR030.

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Introduction Au cours de l’insuffisance respiratoire aiguë (IRA) de novo ou du syndrome de détresse respiratoire aiguë (SDRA), la ventilation invasive (VI) appliquée au patient pour pallier aux altérations sévères de l’hématose, de même que les efforts respiratoires spontanés, peuvent paradoxalement aggraver les lésions alvéolaires initiales et provoquer alors des lésions dénommées ventilator induced lung injury (VILI) ou patient self-inflicted lung injury (P-SILI).L’exacerbation aiguë de pneumopathie interstitielle diffuse (EAPID), bien que proche sémiologiquement, histologiquement et radiologiquement du SDRA et ayant bénéficié de l’amélioration des connaissances du VILI et du P-SILI, reste grevée d’une mortalité bien plus élevée. MéthodeNous nous sommes donc intéressés aux conséquences de la ventilation et des efforts respiratoires spontanés au cours des EAPID.RésultatsNous avons tout d’abord étudié les conséquences des stratégies d’oxygénation non invasives au cours de l’IRA de novo et montré que la ventilation non invasive (VNI) augmentait le volume courant par rapport à l’oxygénothérapie à haut débit (OHD) sans augmentation du recrutement alvéolaire, donc exposant le poumon à un risque de surdistention. Nous avons ensuite mis au point un modèle de poumon artificiel mécanique reproduisant la ventilation spontanée au cours de l’IRA de novo et les mécanismes physiopathologiques impliqués dans le P-SILI.Nous avons ensuite utilisé ces connaissances acquises au cours de l’IRA de novo pour modéliser la ventilation spontanée des patients atteints de PID au repos, au cours d’un exercice maximal et d’une EAPID. Nous avons mis en évidence que l’hétérogénéité de l’atteinte pulmonaire, et donc de la compliance dans les PID, était associée tant à l’effort qu’au cours de l’EAPID à la présence de mécanismes impliqués dans le P-SILI : recrutement/dérecrutement alvéolaires, surdistension, concentration du stress pulmonaire, et phénomène de Pendelluft.Nous avons ensuite soumis ce modèle d’EAPID aux contraintes de la VI. Nous avons ainsi pu montrer que celle-ci, appliquée avec des volumes courants supérieurs à 5 ml/kg de poids prédit sur la taille, des niveaux de pressions expiratoire positive supérieure à 4 cmH2O et une fréquence respiratoire supérieure à 25/min, était potentiellement délétère selon notre modèle. Nous avons parallèlement évalué, au cours d’une étude clinique rétrospective, les conséquences de la stratégie d’oxygénation non invasive appliquée au cours de l’EAPID. A contrario de ce que nous avions pu montrer dans l’IRA de novo, nous n’avons pas retrouvé de différence entre la VNI et l’OHD en termes de mortalité ou de recours à la VI. Grace à notre modèle expérimental d’EAPID, nous devrions pouvoir comprendre les mécanismes physiopathologiques expliquant ce résultat et envisager une stratégie d’oxygénation optimisée et personnalisée pour la prise en charge de l’EAPID. ConclusionNotre travail de recherche, à la fois expérimental et clinique, a donc permis de mettre en évidence la possibilité de P-SILI et de VILI au cours des EAPID, de montrer que le risque de surdistension est majeur dans cette pathologie au cours de la VI. La stratégie d’oxygénation non invasive optimale reste encore à déterminer IntroductionIn the course of de novo acute respiratory failure (ARF) or acute respiratory distress syndrome (ARDS), invasive mechanical ventilation (IMV) and spontaneous respiratory efforts, may paradoxically worsen initial alveolar lesions and cause ventilator induced lung injury (VILI) or patient self-inflicted lung injury (P-SILI). Acute exacerbation of diffuse interstitial lung disease (AE-ILD) presents similar characteristics to ARDS in semiology, histology and radiology. However, the risk of mortality remains higher in AE-ILD despite improved knowledge of VILI and P-SILI. MethodsWe were interested in the effects of ventilation and spontaneous respiratory effort during AE-ILD.ResultsWe first studied the effects of non-invasive oxygenation strategies during de novo ARF, and showed that non-invasive ventilation (NIV) increased tidal volume compared to high flow nasal canulae oxygen therapy (HFNC) without increasing alveolar recruitment, thus exposing the lung to the risk of overdistention. We then developed a mechanical artificial lung model reproducing spontaneous ventilation during de novo ARF and studied the pathophysiological mechanisms involved in P-SILI.We then used this knowledge learned from de novo ARF to model spontaneous ventilation in patients with ILD at rest, during maximal exercise and AE-ILD. We demonstrated that the inhomogeneity of lung injury and of compliance in ILD was associated during exercise and AE-ILD, with the presence of mechanisms involved in P-SILI: recruitment/derecruitment, overdistension, stress concentration and Pendelluft phenomenon.We then exposed this AE-ILD model to the challenges of IMV. We showed that IMV applied with tidal volumes of more than 5 ml/kg PBW, positive expiratory pressure levels of more than 4 cmH2O and respiratory rates of more than 25 cpm were deleterious in our model. At the same time, we evaluated the effects of non-invasive oxygenation strategies during AE-ILD in a retrospective clinical study. We found no difference between NIV and HFNC in mortality or use of invasive ventilation. ConclusionOur research has highlighted the occurence of P-SILI and VILI during AE-ILD and has shown a major risk of overdistension in AE-ILD during IMV. Our model of AE-ILD could help us to develop optimized and personalized oxygenation strategies for AE-ILD patients

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Gaspari, Romolo Joseph. "Pathophysiology of Respiratory Failure Following Acute Organophosphate Poisoning : A Dissertation." eScholarship@UMMS, 2009. https://escholarship.umassmed.edu/gsbs_diss/445.

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Organophosphate (OP) poisoning is a health issue worldwide with over 200,000 deaths per year. Although not a problem in most developed countries, in some third world countries, one third of a hospital’s population could be patients with OP exposure. Even with the most aggressive therapy, 10-40% of patients admitted to an intensive care unit will die. Research into the best practice for treating OP poisoning is lacking, due somewhat to a lack of detailed understanding of the physiology of OP poisoning. Our research uses animal models of acute OP poisoning to explore the mechanism of OP-induced respiratory failure. Our research shows that animals poisoned with dichlorvos demonstrated a uniformly fatal central apnea that, if prevented, was followed immediately by a variable pulmonary dysfunction. Potential mechanisms for dichlorvos-induced central apnea can be divided into direct effects on the central respiratory oscillator (CRO) and feedback inhibition of the CRO. Two afferent pathways that can induce apnea include vagal feedback pathways and feed-forward pathways from the cerebral hemispheres. In our studies we found that vagal feedback and feed forward inhibition from the cerebral hemispheres were not required for OP-induced central apnea. The pre-Botzinger complex in the brainstem is thought to be the kernel of the CRO, but exposure of the pre-Botzinger complex to dichlorvos was not sufficient for apnea. Although OP induced central apnea was uniformly fatal, partial recovery of the CRO occurred post apnea with mechanical ventilation. Central apnea was ubiquitous in our rat poisoning model, but pulmonary dysfunction was extremely variable, with a range of pulmonary effects from fulminate pulmonary failure with prominent pulmonary secretions to no pulmonary dysfunction at all. Vagal efferent activity is involved in neural control of pulmonary tissue but the vagus was not involved in OP-induced pulmonary dysfunction. Anti-muscarinic medications are the mainstay of clinical therapy and are commonly dosed by their effects on pulmonary secretions. Our studies found that atropine (the most common therapeutic agent for OP poisoning) resulted in a ventilation-perfusion mismatch secondary to effects on the pulmonary vasculature.

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Tomii, Keisuke. "Noninvasive ventilation for various types of life-threatening acute respiratory failure." Kyoto University, 2011. http://hdl.handle.net/2433/135384.

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Hammond, Brandon. "Identifying an Oxygenation Index Threshold for Increased Mortality in Acute Respiratory Failure." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/603630.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine. Objectives: To examine current oxygenation index (OI) data and outcomes using EMR data to identify a specific OI values associated with outcome. Methods: Retrospective review of electronic medical record (EMR) data for patients age 1 month ‐ 20 years mechanically ventilated for >24 hours in the PICU. Serial, average and maximum OI values were calculated. Length of mechanical ventilation, hospital stay and outcome were assessed. Results: OI was calculated on 65 patients from EMR data, of which 6 died (9.2%). The median maximum OI was 10 for all patients, 17 for non‐survivors (NS), and 8 for survivors (S), (p=0.14 via Wilcoxon rank‐sum test). Odds ratios (OR) indicated 2.1 times increase odds of death (p=.08), 95% confidence interval (0.89–5.03) for each one‐percent increase in maximum OI. Average OI OR also revealed 2.1 times increase in odds of death (p=.14), 95% confidence interval (0.77–5.48). ROC analysis indicated a higher discriminate ability for max OI (AUC = 0.68) than average OI (AUC = .58). OI cut points for mortality were established. Mortality was unchanged until max OI >17, for which mortality nearly tripled at a value of 18% versus 6‐7% for range 0‐17. Conclusions: Serial assessment of OI values may allow creation of alert values for increased mortality risk and aid in development of clinical decision rules. Consideration for escalation of therapies for respiratory failure such as high frequency ventilation or ECMO at lower levels of OI than historically reported may be warranted. This study also helps to validate prior reports that OI is useful as a severity score for clinical research and outcome prediction.

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Nelson, Diane L. "Pulmonary Drug Delivery via Reverse Perfluorocarbon Emulsions: A Novel Method for Bacterial Respiratory Infections and Acute Respiratory Failure." Research Showcase @ CMU, 2018. http://repository.cmu.edu/dissertations/1147.

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Inhaled drug delivery is currently the gold standard for treating many respiratory diseases. However, improved treatments are needed for lung diseases like Cystic Fibrosis (CF) and Acute Respiratory Distress Syndrome (ARDS), where mucus or fluid build-up in the lung limits ventilation and, thus, delivery of inhaled drugs. Delivery is most needed in the diseased or damaged regions of the lung, but if an area is not ventilated, inhaled drug will simply not reach it. To overcome this, this research proposes delivering drugs to the lungs within a perfluorocarbon (PFC) liquid. The lungs will be filled with a reverse emulsion containing a disperse phase of aqueous drugs within the bulk PFC and then ventilated. The PFC functions as both a respiratory medium, providing gas exchange, and as a delivery vehicle, providing a more uniform deposition of drugs. After treatment, the highly volatile PFCs are exhaled, returning the patient to normal respiration. This technique improves upon current therapies as follows. First, drugs are delivered directly to where they are needed, yielding higher concentrations in the lung and lower systemic concentrations. Second, PFCs are ideal for washing out lung exudate and mucus. The low surface tension and high density of PFC allows it to easily penetrate plugged or collapsed alveoli, detach infected mucus from the airway walls, and force these fluids to the top of the lungs where they can then be removed via suction. Mucus and exudate removal should allow drugs to penetrate previously plugged airways during emulsion delivery and subsequent treatment with inhaled therapies. Thus, drug delivery via emulsion would be used as a pre-treatment to enhance inhaled or systemic drug therapy. Third, PFC’s anti-inflammatory properties help return to normal lung function. This research examines two applications of this technology: delivery of antibiotics to combat respiratory infections (antibacterial perfluorocarbon ventilation, APV) or delivery of growth factors to enhance alveolar repair (perfluorocarbon emulsions for alveolar repair, PEAR). This work represents an in-depth analysis of the emulsions used during APV and PEAR. Initial efforts evaluated emulsion efficacy under in vitro setting that better simulated lung in vivo antibiotic delivery. The subsequent studies utilized an in vivo rat model of bacterial respiratory infection to validate the effects of emulsion on pharmacokinetics and to assess APVs potential treatment benefits. Lastly, in vitro methods of cellular response assessed the utility of delivering growth factors in PEAR. Significant advancements were made in optimizing the emulsion as a viable means of pulmonary drug delivery. Final efforts resulted in a promising emulsion formulation that overcame the quick transport of tobramycin away from the lung and successfully reduced pulmonary bacterial load in vivo. In vitro applications of PEAR showed the emulsions posed a significant barrier to the availability and, thus, the biological effect of lysophosphatidic acid growth factors. Further in vivo work is required to improve APV’s efficacy over conventional treatments and to determine PEAR’s feasibility and efficacy in promoting lung repair.

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Boyarskiy, O. O., O. O. Tikhonova, G. O. Solomennyk, and O. I. Mohylenets. "Features of acute respiratory viral infections in patients with congenital syndrome of immune-endocrine failure." Thesis, Sumy State University, 2016. http://essuir.sumdu.edu.ua/handle/123456789/47814.

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Congenital syndrome of immune-endocrine insufficiency (CSIEI) is the type of constitution that is morphologically characterized by primary hyperplasia of the thymus, generalized hyperplasia of lymphoid tissue, adrenal hypoplasia in combination with various anomalies of cardiovascular, and less frequently of urogenital systems. Features of CSIEI in a functional sense are the failure of infectious and immune violations of adaptation under stress. Endocrine failure, which occurs in patients with CSIEI, usually go unnoticed in the outpatient setting and in the ICU appears addisonian crisis with hypovolemia and shock, which are resistant to treatment. Objective: to develop criteria for lifetime diagnosis and prevention CSIEI.

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ZAMBELLI, VANESSA. "Pet imaging for evaluation of inflammatory response in a murine model of acute respiratory failure." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/43295.

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Background: Acute Respiratory Distress Syndrome (ARDS) is a life-threatening form of acute respiratory failure, with a still high mortality. Aspiration pneumonitis is a clinical disorder that, entailing a direct lung injury, is associated to ARDS. It is characterized by an acute inflammatory response with neutrophilic recruitment into the lung and a late fibrotic evolution of injury. This study investigates whether the use of PET could allow to monitor this inflammatory response and its correlation with the later fibroproliferative phase in an experimental model of acute respiratory failure. Since to date no specific therapeutic strategies are available for ARDS patients, we tested the effects of exogenous surfactant treatment on lung injury evolution, by monitoring it with CT-PET imaging. Methods: Hydrochloric acid (0,1M) was instilled (1,5 ml/kg) into the right bronchus of mice. The study was divided into three parts. Time-course experiment: four groups of mice underwent micro-CT and micro-PET scans and sacrificed at different time point (6hrs, 24 hrs, 48 hrs and 7 days after surgery) to assess arterial blood gases, histology and bronchoalveolar lavage (BAL). Long-term experiment: one group of mice underwent a micro-CT scan 1 hour after lung injury and a series of [18F]FDG-PET at the same time points. 21 days after respiratory static compliance was measured and lung tissue was collected in order to measure the OH-proline content. Treatment experiment: two groups of mice were treated with exogenous surfactant (Curosurf ®) or vehicle (sterile saline 0.9 %) three hours after HCl instillation. Animals underwent micro-CT and a series of micro-PET scans. 21 days after they were sacrificed to measure lung mechanics and collagen deposition. Results: Histological analysis showed a rapid recruitment of neutrophils into the damaged lung 6 hours after injury, with a peak after 24 hours. Macrophages, as expected, reached the peak after 48 hours. [18F]FDG signal, as inflammation marker, showed similar time course to that of recruited inflammatory cells (sum of two cell types). Mice that were sacrificed 21 days after the surgery were characterized by a correlation between a reduced respiratory static compliance and a high PET signal 7 days after lung injury. PET signal correlated also with collagen content. This correlation was confirmed in treatment experiment, in which we found that exogenous surfactant administration improved lung fibrotic evolution, by reducing collagen deposition. Conclusions: This study demonstrated the possibility to use PET imaging to follow the inflammatory response also in longitudinal studies. Moreover a correlation between a persistence of inflammatory process and fibrotic evolution was showed. We speculate that it is possible that acute treatments of the inflammation capable of reducing the fibroproliferative process, could be monitored using the FDG-PET method.

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Van, der Schyff Nasief. "Risk factors for prolonged ventilation in patients with chronic obstructive pulmonary disease presenting with acute respiratory failure." Master's thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/12112.

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Includes abstract. Includes bibliographical references (leaves 35-37). Patients with COPD presenting to the Emergency Unit with acute hypercapnic respiratory failure often require invasive mechanical ventilation and subsequent admission to the intensive care unit (ICU). These patients are at an increased risk of prolonged and complicated ventilation and often experience weaning difficulties. In addition, the impact of a previous episode of pulmonary tuberculosis that might have resulted in structural lung disease on the duration of mechanical ventilation in such patients has not previously been evaluated. Methods: All patients with COPD admitted to the Respiratory ICU at Tygerberg academic hospital from the 01st January 2004 until 31st December 2007 requiring intubation and invasive mechanical ventilation for acute hypercapnic respiratory failure were included in the study.

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Balfour, Liezl. "Development of a clinical pathway for non-invasive ventilation in a private hospital in Gauteng." Diss., University of Pretoria, 2011. http://hdl.handle.net/2263/30377.

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Despite the advantages of using NIV, healthcare professionals are not in agreement about precisely when to commence NIV (Elliott, Confalonieri& Nava 2002:1159; Lightowler, Wedzicha, Elliott&Ram 2003: [4]; Garpestad &Hill 2006:147), which adds to the underutilisation of NIV. The aim of this study was to collaboratively develop a clinical pathway for NIV. Two main objectives were identified, namely (i) to identify the components of a clinical pathway for NIV, and (ii) to develop a clinical pathway for NIV that can be implemented in the CCU. The research design utilised for this study was qualitative, contextual, explorative and descriptive in nature. The study consisted of three phases, namely Phase 1: Components of the clinical pathway, Phase 2: Literature control, and Phase 3: Development of the clinical pathway. The objectives of the study were met, and a clinical pathway for NIV was developed. Dissertation (MCur)--University of Pretoria, 2011. Nursing Science unrestricted

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Steinhorst, Renata Campos. "Influência dos procedimentos hemodialíticos na mecânica respiratória em pacientes com insuficiência renal, aguda ou crônica, sob ventilação mecânica invasiva." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-04012007-170650/.

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Introdução: A insuficiência renal (IRen) aguda ou renal crônica podem levar a complicações respiratórias, que podem culminar com insuficiência respiratória aguda (IRpA), severa hipoxemia e alterações de mecânica respiratória (MR). O tratamento hemodialítico, pode desencadear um processo inflamatório pulmonar entretanto, a correção da hipervolemia que proporciona, pode melhorar a IRpA. O objetivo deste estudo foi avaliar a influência da hemodiálise (HD) na MR de pacientes com IRen sob ventilação mecânica invasiva (VMI). Materiais e Métodos: Pacientes com IRen, idade 18 a 75 anos, em VMI e em HD. Parâmetros analisados: clínicos gerais, laboratoriais (hemograma, gasometria arterial, função renal), características da HD e MR (complacência estática e dinâmica, e resistência do sistema respiratório). Os parâmetros foram analisados antes do início da HD e 4 horas após seu início. Resultados: (média ± DP) Foram analisados 37 pacientes, idade 51 ± 17 anos. Houve perda de peso, e melhora dos parâmetros laboratoriais (p < 0,05) exceto a PaO2 e a saturação de O2. A HD não alterou a pressão arterial e nem a MR, porém o delta da complacência dinâmica apresentou correlação com o delta de creatinina (p = 0,02). Conclusão: A HD por 4 horas não altera a MR de pacientes sob VMI. Introduction: Renal failure (RF), acute or chronic, can induce respiratory complications that can evolve to acute respiratory failure (ARpF), hypoxemia and severe changes in respiratory mechanics (RM). Hemodialysis (HD) can produce pulmonary inflammation and worse the ARpF. On other hand, HD corrects hypervolemia and thus can improve the ARpF. The objective of this study was evaluating the HD role in RM of RF patients in use of invasive mechanical ventilation (IMV). Materials and Methods: Patients with RF, age 18 to 75 years, in use of IMV and HD. Analyzed parameters: age, gender, HD characteristics, respiratory and renal laboratory tests, and RM evaluation (static and dinamic compliance and resistence). Parameters were evaluate before HD and 4 hours after it started. Results (mean ± SD): We studied 37 patients, age 51 ± 17 years. During HD the patients lost body weight and presented an improvement in pulmonary and renal parameters (p < 0.05) except for PaO2 and arterial O2 saturation (p > 0.05). HD did not induce hemodynamic instability. There was correlation (p = 0.02) between the changes in plasma creatinine and the changes in dynamic compliance. Conclusion: HD for 4 hours did not modify respiratory mechanics in patients in use of IMV.

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Książki na temat "De novo acute respiratory failure"

1942-, Zapol Warren M., and Falke Konrad J, eds. Acute respiratory failure. Dekker, 1985.

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C, Bone Roger, George Ronald B, and Hudson Leonard D. 1938-, eds. Acute respiratory failure. Churchill Livingstone, 1987.

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Vincent, Jean Louis, and Peter M. Suter, eds. Cardiopulmonary Interactions in Acute Respiratory Failure. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83010-5.

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Jean-Philippe, Derenne, Similowski Thomas 1961-, and Whitelaw William A. 1941-, eds. Acute respiratory failure in chronic obstructive pulmonary disease. M. Dekker, 1996.

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Enright, Stephanie. Cardiorespiratory alterations following positional adjustment in critically ill mechanically ventilated patients with acute respiratory failure. University of Manchester, 1997.

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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.

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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.

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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.

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Cardiopulmonary interactions in acute respiratory failure. Springer-Verlag, 1987.

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Cardiopulmonary Interactions in Acute Respiratory Failure. Springer, 2011.

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Wise, Matt, and Simon Barry. Respiratory failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0135.

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Respiratory failure is a syndrome characterized by defective gas exchange due to inadequate function of the respiratory system. There is a failure to oxygenate blood (hypoxaemia) and/or eliminate carbon dioxide (hypercapnia). Hypoxaemia is defined as an arterial blood partial pressure of oxygen (PaO2) of <8 kPa, and hypercapnia as an arterial blood partial pressure of carbon dioxide (PaCO2) of >6 kPa. Respiratory failure is divided into two different types, conventionally referred to as type 1 and type 2. The distinction between these two is important because it emphasizes not only different their pathophysiological mechanisms and etiologies, but also different treatments. The preferred terminology and definitions are as follows: oxygenation failure (type I respiratory failure), PaO2 of <8 kPa; ventilation failure (type 2 respiratory failure), PaCO2 >6 kPa. Respiratory failure may be acute (onset over hours to days), or chronic (developing over months to years); alternatively, there may be an acute deterioration of a chronic state.

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Części książek na temat "De novo acute respiratory failure"

Bshesh, Khalid K., and Manal Alasnag. "Acute Respiratory Failure." In Textbook of Clinical Pediatrics. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_266.

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Rehder, Kyle J., Jennifer L. Turi, and Ira M. Cheifetz. "Acute Respiratory Failure." In Pediatric Critical Care Medicine. Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6362-6_31.

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Caruso, Lawrence J., and T. James Gallagher. "Acute Respiratory Failure." In Surgical Intensive Care Medicine. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4757-6645-5_20.

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Mador, M. J., and M. J. Tobin. "Acute Respiratory Failure." In Chronic Obstructive Pulmonary Disease. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-4525-9_19.

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Mosier, Jarrod M. "Acute Respiratory Failure." In Emergency Department Critical Care. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-28794-8_3.

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Peter, John Victor. "Acute Respiratory Failure." In Clinical Pathways in Emergency Medicine. Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2710-6_13.

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Guleria, Randeep, Jaya Kumar, and Rajesh Chawla. "Acute Respiratory Failure." In ICU Protocols. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-0898-1_2.

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Gattinoni, Luciano, Eleonora Carlesso, and Federico Polli. "Acute Respiratory Failure." In Surgical Intensive Care Medicine. Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-77893-8_22.

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Champion, Howard R., Nova L. Panebianco, Jan J. De Waele, et al. "Acute Respiratory Failure." In Encyclopedia of Intensive Care Medicine. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1085.

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Guleria, Randeep, and Jaya Kumar. "Acute Respiratory Failure." In ICU Protocols. Springer India, 2012. http://dx.doi.org/10.1007/978-81-322-0535-7_2.

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Streszczenia konferencji na temat "De novo acute respiratory failure"

Artaud Macari, Elise, Emeline Fresnel, Adrien Kerfourn, et al. "Modeling lung ventilation in de novo acute respiratory failure: a bench study." In ERS International Congress 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/13993003.congress-2023.pa1212.

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Coudroy, R., M. A. Hoppe, R. Robert, F. Jean-Pierre, and A. W. Thille. "Influence of the Noninvasive Ventilation Protocol on Intubation Rate in Patients with De Novo Acute Respiratory Failure: A Systematic Review of Randomized Trials." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1614.

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Demoule, A., A. Baptiste, A. Thille, et al. "Dyspnea Is Associated With a Higher Intubation Rate and Mortality in De Novo Acute Hypoxemic Respiratory Failure - A Secondary Analysis of a Randomized Trial." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1707.

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Ketcham, S., Y. R. Sedhai, H. C. Miller, et al. "Dying with Respiratory Failure, Not from Respiratory Failure: Characteristics of Death in Acute Hypoxemic Respiratory Failure and the Acute Respiratory Distress Syndrome." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1139.

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Combes, Alain, Matthieu Schmidt, Nicolas Brechot, et al. "Venovenous ECMO For Acute Respiratory Failure." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6017.

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Sidhom, Samy, Aylin Ozsancak Ugurlu, Ali Khodabandeh, Phil Alkana, Vinay Maheshwari, and Nicholas S. Hill. "Predictors Of Noninvasive Ventilation Failure In Acute Respiratory Failure." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6238.

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Khalaf, Fatema, and Subhashini S. Baskaran. "Predicting Acute Respiratory Failure Using Fuzzy Classifier." In 2023 International Conference on IT Innovation and Knowledge Discovery (ITIKD). IEEE, 2023. http://dx.doi.org/10.1109/itikd56332.2023.10099746.

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Chauhan, S., Q. Abdiani, R. Dadhwal, and A. Shalonov. "Acute Respiratory Failure Associated with Neuromyelitis Optica." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2401.

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Ishikawa, Oki, Matthew Ballenberger, Brian Birnbaum, et al. "HACOR in Action: Noninvasive Ventilation Failure in Acute Respiratory Failure." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1961.

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Neiva Machado, João Pedro, José Coutinho Costa, and Teresa Costa. "Non-invasive ventilation in acute and acute-on-chronic respiratory failure in a respiratory ward." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2163.

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Raporty organizacyjne na temat "De novo acute respiratory failure"

Kuzmin, Vyacheslav, Alexander Kulikov, Alexander Levit, Vladimir Rudnov, Alabai Sabitov, and Rustam Mukhametshin. Electron training course "Intensive therapy of acute respiratory failure in the conditions of a coronavirus pandemic". SIB-Expertise, 2022. http://dx.doi.org/10.12731/er0653.15122022.

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Актуальность дополнительной профессиональной образовательной программы повышения квалификации врачей по теме «Интенсивная терапия острой дыхательной недостаточности в условиях коронавирусной пандемии» обусловлена необходимостью обучения специалистов здравоохранения навыкам своевременного выявления, диагностики и оказания медицинской помощи пациентам, инфицированным COVID-19

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Sanguanwong, Natthawan, Nattawat Jantarangsi, Natthida Owattanapanich, and Vorakamol Phoophiboon. Effect of non-invasive ventilation and high flow nasal cannula on interstitial lung disease with acute respiratory failure: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.6.0104.

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Review question / Objective: P: Interstitial lung disease patient who is suffering with acute respiratory failure. I: Non-invasive oxygen therapy either non-invasive ventilation (NIV) or high flow nasal cannula (HFNC). C: 1. Conventional oxygen therapy, 2. NIV vs HFNC. O: P/F ratio improvement, PaCO2 reduction, mortality, intubation rate. Condition being studied: The benefit of using either non-invasive ventilation or high flow nasal cannula on interstitial lung disease with acute respiratory failure.

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Kang, Hanyujie, Xueqing Gu, and Zhaohui Tong. Effect of awake prone positioning in non-intubated COVID-19 patients with acute hypoxemic respiratory failure: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2021. http://dx.doi.org/10.37766/inplasy2021.11.0037.

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Teng, Wenzhe, Hu Chen, Siyao Shi, Yin Wang, and Kangyao Cheng. Effect of bilevel continuous positive airway pressure for patients with type II respiratory failure due to acute exacerbation of COPD: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2020. http://dx.doi.org/10.37766/inplasy2020.11.0003.

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F, Verdugo-Paiva, Izcovich A, Ragusa M, and Rada G. Lopinavir/ritonavir for COVID-19: A living systematic review. Epistemonikos Interactive Evidence Synthesis, 2024. http://dx.doi.org/10.30846/ies.4f3c02f030.v1.

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Objective Provide a timely, rigorous, and continuously updated summary of the evidence on the role of lopinavir/ritonavir in the treatment of patients with COVID-19. Methods We conducted searches in the special L.OVE (Living OVerview of Evidence) platform for COVID-19, a system that performs regular searches in PubMed, Embase, CENTRAL, and other 33 sources. We searched for randomized trials and non-randomized studies evaluating the effect of lopinavir/ritonavir versus placebo or no treatment in patients with COVID-19. Two reviewers independently evaluated potentially eligible studies, according to predefined selection criteria, and extracted data using a predesigned standardized form. We performed meta-analyses using randomeffect models and assessed overall certainty in evidence using the GRADE approach. A living, web-based version of this review will be openly available during the COVID-19 pandemic. Results Our search strategy yielded 862 references. Finally, we identified 12 studies, including two randomized trials, evaluating lopinavir/ritonavir, in addition to standard care versus standard care alone in 250 adult inpatients with COVID-19. The evidence from randomized trials shows lopinavir/ritonavir may reduce mortality (relative risk: 0.77; 95% confidence interval: 0.45 to 1.3; low certainty evidence), but the anticipated magnitude of the absolute reduction in mortality, varies across different risk groups. Lopinavir/ritonavir also had a slight reduction in the risk of requiring invasive mechanical ventilation, developing respiratory failure, or acute respiratory distress syndrome. However, it did not lead to any difference in the duration of hospitalization and may lead to an increase in the number of total adverse effects. The overall certainty of the evidence was low or very low. Conclusions For severe and critical patients with COVID-19, lopinavir/ritonavir might play a role in improving outcomes, but the available evidence is still limited. A substantial number of ongoing studies should provide valuable evidence to inform researchers and decision-makers soon Keywords COVID-19, Severe acute respiratory syndrome coronavirus 2, Coronavirus Infections, Systematic review, Lopinavir, Lopinavir/ritonavir, Antivirals

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Pre-hospital non-invasive ventilation for people with acute respiratory failure. National Institute for Health Research, 2015. http://dx.doi.org/10.3310/signal-000107.

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