Bar de Oxigênio / Oxigenoterapia

[Dellbono]

lol cara, o Dellbono tava em La Paz, com falta de oxigênio, é óbvio que ele se sentiu melhor inalando oxigênio neh!

Foi mais ou menos isso mesmo.
Estávamos a trabalho , aí o meu amigo passou muito mal e começou a sentir ânsia
de vômito.
Liguei para recepção e pedi ajuda.

5 minutos depois apareceu um camareiro com um cilindro pequeno num carrinho e duas máscaras.
Disse que estávamos sentido o efeito da altitude e que inalar o oxigênio ia aliviar.

Foi engraçado porque perguntamos quanto ia custar aquela gentileza e ele disse:

- O 1º tubo é cortesia do hotel. A partir do 2º cobramos 25 dólares!

É exatamente o que o Alvinho falou, eu me senti melhor porque estava com dificuldades para respirar.
Teve um jogo do Flamengo que a comissão técnica ficou com uns tubos na beira do campo e alguns jogadores iam até a lateral para inalar oxigênio.

Já ouvi falar , até mesmo em seriados e filmes, que os cassinos utilizam o recurso de oxigenar o ambiente
através dos dutos de ar condicionado afim de proporcionar uma sensação de leve euforia aos seus clientes.

Daí a querer comprar ou alugar um tubo de oxigênio só para curtir um barato me parece meio louco.
Seria legal os médicos do fórum opinarem sobre os reais efeitos e riscos da inalação de oxigênio extra.
@Ljc

[Alvinho]

é mito essa parada do cassino

[Soneca]

"INTRODUCTION — Although supplemental oxygen is valuable in many clinical situations, excessive or inappropriate supplemental oxygen can be deleterious [1]. According to human and animal studies, high concentrations of inspired oxygen can cause a spectrum of lung injury, ranging from mild tracheobronchitis to diffuse alveolar damage (DAD) [2-6]. The latter is histologically indistinguishable from that observed in the acute respiratory distress syndrome (ARDS). The mechanisms and clinical consequences of oxygen toxicity are reviewed here. Specific issues related to the administration of oxygen are discussed separately. (See "Use of oxygen in patients with hypercapnia" and "Long-term supplemental oxygen therapy".)CELLULAR INJURY — Hyperoxia is poorly defined, but probably exists whenever oxygen tension exceeds 21 percent of atmospheric pressure. It appears to produce cellular injury through increased production of reactive oxygen species, such as the superoxide anion, the hydroxyl radical, and hydrogen peroxide [7,8]. When the production of these reactive species increases and/or the cell's antioxidant defenses are depleted, oxygen radicals can react with and impair the function of essential intracellular macromolecules, resulting in cell death [9].
Oxygen free radicals may also promote a deleterious inflammatory response, leading to secondary tissue damage and/or apoptosis [10-12]. Support for the role of reactive oxygen species in producing cellular injury has come from studies in transgenic mice with altered superoxide dismutase activity. Mice with augmented antioxidant mechanisms have a relative tolerance to hyperoxia, while manganese superoxide dismutase knockout mice die shortly after birth with extensive mitochondrial injury within degenerating neurons and cardiac myocytes [13-15].
Lung tissue is exposed to the highest concentrations of oxygen in the body, placing cells that line the tracheobronchial tree and alveoli at the greatest risk for hyperoxic cytotoxicity [16]. Hyperoxia may also increase susceptibility to mucous plugging, atelectasis, and secondary infection by impairing both mucociliary clearance and the bactericidal capacity of immune cells [17-22].
CLINICAL CONSEQUENCES — High fractions of inspired oxygen (FiO₂) have been associated with several pulmonary consequences: increased intrapulmonary right-to-left shunt fraction and diminished lung volumes due to absorptive atelectasis; accentuation of hypercapnia; and damage to airways and pulmonary parenchyma. The term "oxygen toxicity" is usually reserved for the last of these consequences, ie, tracheobronchial and pulmonary parenchymal damage.
Absorptive atelectasis — High concentrations of supplemental oxygen cause washout of alveolar nitrogen (ie, oxygen replaces nitrogen in the alveolus). This may cause absorptive atelectasis if oxygen diffuses from the alveoli to the capillaries faster than it is replenished by inhaled oxygen. Absorptive atelectasis is theoretically more likely in the following circumstances:

• A low regional ventilation-perfusion ratio, which limits replenishment of alveolar oxygen (in general, airway closure is required for this mechanism to be important)
• Qualitative or quantitative surfactant abnormalities that promote alveolar collapse and further reduce the ventilation-perfusion ratio
• A high rate of oxygen uptake, due to an increase in metabolic demand
• An impaired pattern of respiration that fails to correct atelectasis (eg, ventilation at low tidal volumes and/or without intermittent sighs)

Shunting resulting from absorptive atelectasis is minor in younger patients, but can rise to as high as 11 percent in older, otherwise healthy volunteers breathing 100 percent oxygen for 30 minutes (calculator 1) [23].
Once well established, absorptive atelectasis is not rapidly reversed by a reduction of FiO₂ to maintenance levels, emphasizing the desirability of rapid titration of FiO₂ to the lowest fraction necessary to maintain an SaO₂ >90 percent [24].
Decrements in vital capacity of up to 20 percent have been noted after hyperoxic exposure in a number of experiments [2,17]. This is presumably due to a combination of absorptive atelectasis and shallow breaths secondary to pleuritic pain from tracheobronchitis.
Accentuation of hypercapnia — Hyperoxic hypercarbia describes the phenomenon of increased PaCO₂ associated with increases in FiO₂ in individuals with chronic compensated respiratory acidosis. In general, the increased hypercapnia does not lead to CO₂ narcosis and respiratory failure, because the relative rise in PaCO₂ is small and these patients are acclimatized to their higher baseline level of PaCO₂. (See "Use of oxygen in patients with hypercapnia".)
Several mechanisms act in concert to produce hyperoxic hypercapnia, including [25-27]:

• The Haldane effect. The rightward displacement of the CO₂-hemoglobin dissociation curve in the presence of increased oxygen saturation. This occurs because oxyhemoglobin binds CO₂ less avidly than deoxyhemoglobin, thereby increasing the amount of CO₂ dissolved in blood, which in turn determines PaCO₂.
• An increase in dead space (ie, "wasted") ventilation. This probably reflects worsening ventilation-perfusion matching and redistribution of blood flow from well-ventilated to poorly ventilated alveoli due to a loss of hypoxic pulmonary vasoconstriction. Carbon dioxide-induced bronchodilation may also be important in mediating the increase in dead space [28].
• A modest decrease in minute ventilation due to decreased stimuli from peripheral chemoreceptors to the central respiratory center. (See "Control of ventilation".)
• The anxiolytic and anti-dyspneic effects of supplemental oxygen can promote sleep, particularly in patients who arrive in the emergency department sleep-deprived. The onset of sleep is associated with loss of the voluntary drive to breath. When the behavioral influences on breathing present during wakefulness are absent, respiration is sustained solely by metabolic control mechanisms. This can result in progressive hypercarbia [29,30].
• Hypoventilation decreases inspiratory flow demand, which reduces the amount of room air entrained around a face mask or nasal cannula. This may increase the FIO₂ delivered to the patient, even if the flow rate from the oxygen source is unchanged [29]. The net effect is supplementation of the causes of hypercapnia, which were discussed above.

Airway injury — Many healthy volunteers experience substernal heaviness, pleuritic chest pain, cough, and dyspnea within 24 hours of breathing pure oxygen; these symptoms are probably due to a combination of tracheobronchitis and absorptive atelectasis [31]. Erythema and edema of large airways can be observed bronchoscopically in most patients treated with a FiO₂ of 0.9 for six hours and are thought to reflect hyperoxic bronchitis [32]. In addition, the concentration of reactive oxygen species in exhaled gas increases after only one hour of breathing 28 percent oxygen, regardless of the presence of underlying lung disease [33].
Bronchopulmonary dysplasia (BPD), a disease seen in neonates following recovery from neonatal respiratory distress syndrome, has been attributed to the effects of mechanical ventilation and oxygen toxicity in the immature lung. BPD is characterized by epithelial hyperplasia and squamous metaplasia in the large airways, thickened alveolar walls, and peribronchial and interstitial fibrosis. Infants with BPD generally suffer respiratory distress and require supplemental oxygen for up to six months. (See "Pathogenesis and clinical features of bronchopulmonary dysplasia".)
Parenchymal injury — Progressive worsening of airspace disease can be observed in patients with ARDS who are sustained on mechanical ventilation, and may be due to progression of the underlying process that produced ARDS, development of ventilator-associated pneumonia, ventilator-induced lung injury secondary to mechanical forces, or DAD from the toxic effects of oxygen. Determining the magnitude of parenchymal injury due solely to oxygen therapy in humans is problematic because confounders are usually present. Many of the limited human data on hyperoxic pulmonary injury are from healthy volunteers, and their relevance to actual clinical settings is debatable.
Several studies involving patients in critical care units have attempted to assess the clinical significance of pulmonary oxygen toxicity but have yielded conflicting results:

• One prospective study randomized 40 patients undergoing cardiac surgery to postoperative treatment with either 100 percent oxygen via an endotracheal tube for a mean of 24 hours, or to the minimum FiO₂ required to maintain an arterial oxygen tension of 80 to 120 mmHg [34]. Despite the differences in FiO₂ exposure, there was no difference in right-to-left shunt fraction, effective compliance, or dead space to tidal volume ratio between the two groups.
• A second report randomized 10 patients with irreversible brain damage to either 21 percent or 100 percent oxygen for a mean of 52 hours and noted substantial deterioration in the hyperoxic group in terms of decreased PaO₂, increased right-to-left shunt fraction, and increased dead space to tidal volume ratio [35]. However, postmortem examination of the lungs revealed no major histopathologic differences (including no hyaline membranes characteristic of early DAD) among the two treatment groups.
  
  The physiologic deterioration in the hyperoxic patients in the second study may have reflected progressive absorptive atelectasis, which was less prominent in the first series because patients were exposed to hyperoxia for shorter periods of time and had spontaneous respiratory efforts. Alternatively, physiologic changes associated with brain injury or cardiac surgery may explain the apparent differences in behavior of these two populations. (See "Neurogenic pulmonary edema".)
• A retrospective study of 16 previously healthy, nonsmoking survivors of ARDS found that treatment with an FiO₂ >0.6 for more than 24 hours was both a sensitive and specific predictor of a reduced diffusing capacity (DLCO) at one year [36]. Although there were potential biases in this study based on severity of illness (patients with more biologically severe ARDS presumably received higher concentrations of oxygen), the duration of FiO₂ >0.6 was the only variable which predicted the degree of diffusing abnormality.

Potentiation by bleomycin — Patients who receive bleomycin appear to be more susceptible to diffuse alveolar damage following oxygen exposure, based upon in vitro data and uncontrolled clinical experience [37]. The typical presentation of combined bleomycin/oxygen toxicity involves a patient with testicular cancer or Hodgkin lymphoma who, after receiving bleomycin, requires supplemental oxygen due to aspiration, pneumonia, or general anesthesia. Following oxygen administration, the patient develops subacute worsening of bilateral alveolar infiltrates with increasing dyspnea, nonproductive cough, and decreasing lung compliance. (See "Bleomycin-induced lung injury".)
The diagnosis of this syndrome is established by the exclusion of other processes such as heart failure, worsening pneumonia, ongoing aspiration, or alveolar hemorrhage. Lung injury associated with amiodarone or external beam radiation may involve oxygen radicals in its pathogenesis, and also may predispose individuals to hyperoxic complications. (See "Amiodarone pulmonary toxicity" and "Radiation-induced lung injury".)
Extrapulmonary toxicity — The retinopathy of prematurity (previously called retrolental fibroplasia) has been attributed to the toxic effects of oxygen. One cohort study of 101 infants demonstrated a significant association between the duration of transcutaneously measured PaO₂ >80 mmHg and the incidence and severity of retinopathy [38]. Central nervous system symptoms, including generalized tonic-clonic seizures, have been reported secondary to hyperoxia but are unusual in the absence of hyperbaric therapy. (See "Retinopathy of prematurity".)
Hyperoxia may also alter cardiovascular function [39,40]. Increased oxygen tension can lead to local coronary vasoconstriction, and microscopic foci of myocardial necrosis have been observed in animal models [41]. Reductions in stroke volume and cardiac output, relative bradycardia, and an increase in systemic vascular resistance may ensue, but the clinical relevance of hyperoxia-related hemodynamic effects remains unclear [42].
"

Se alguém quiser ler...

Pra quem não quer, fica só a primeira frase:
"Although supplemental oxygen is valuable in many clinical situations, excessive or inappropriate supplemental oxygen can be deleterious [1]."

- Embora suplementação de oxigênio seja valiosa em diversas situações clínicas, seu uso excessivo ou inapropriado pode ser deletério.

(cortei uns pedaços pra poder postar)

[rzen]

oxigenio melhora o humor sim, e dá um animo a mais, mas é que nem café... uma hora vc acaba ficando resistente aos efeitos, e talvez até se sinta pior sem. O melhor jeito de conseguir de graça é indo num hospital publico e dizer que está tendo uma crise de asma, se não tiver ninguem olhando, vc pode abrir um pouco a torneirinha do no2 que dá um elo melhor que o 02

O cara já deu mostras que realmente quer a parada: já foi em inúmeros médicos só por causa disso, pesquisou no google, se dispõe a gastar $ nisso... Dai vc sugere a ele a simular uma doença pra ocupar um leito de um hospital público desnecessariamente? Tá sobrando vaga nos hospitais, né?

Sério, puta merda, que grande desserviço, hein... Não duvido nada do op tentar isso mesmo

Lógico que nem penso em tentar isso. Já pedi em hospital particular mas falaram que só com recomendação médica, o que não consegui.

Simular doença tb não passa pela cabeça, agora não vejo ser tão errado assim conseguir uma inalação em hospital
público, afinal com o imposto que a gente paga eles deveriam doar 1 cilindro carregado.

[rzen]

Falei com um cara da white martins e diz que eles entregam em casa, mas normalmente é para senhoras de 95 anos.
Mas esses são iguais aos dos hospitiais, concentração aprox. = 93%.
@Jhonny, então melhor comprar um desse:

CPAPMed - Equipamentos Médicos

Mas também nunca usei, só que estou curioso, mesmo que não comprovaram se traz benefício no longo prazo, algumas pessoas reportaram que se sentiram melhor.

O próprio @Dellbono confirmou aqui.

qto custa esse?
parece ser caro

Aprox. R$ 3k, mas não precisa carregar, pois é um concentrador.
Aquelel do aluguel em sp pode acabar saindo mais caro e deve ter concentração bem menor.

[rzen]

"Todos falaram que não era o caso e que a única coisa que poderia acontecer era eu ficar tonto."

Nenhum deles errou...

Pode ser que sim, mas não tem como ter ctza, talvez com uma amostragem maior.

Fui em 3 médicos esses tempos e cada 1 deu uma resposta diferente pro mesmo problema que falei,
inclusive indicaram tratamento/respostas diferentes, então é bem subjetivo mesmo.

[rzen]

é mito essa parada do cassino

Tb não acredito que "jogam oxigênio" no ar, mas que tem disponível para quem quiser e obv que
acreditam que tem algum benefício como manter os gamblers mais acordados e propensos a apostar.

Sobre o WSOP/RIO:

QUOTE
Speaking of oxygen, if you're in need of a boost of fresh air, there's an oxygen bar in the hallways of the Rio.

The next step is the WSOP hallway. Here, everything from oxygen to books are being sold to enthusiastic players and tourists.

Why he can afford a $1M buy-in: Increased oxygen levels and free cocktails clouded his judgment, stopping him from leaving the casino mid-heater.

UNQUOTE

[Jhonny]

São Paulo Oxigênio | 24 horas

Acabei de ligar , e o rapaz me falou que a compra d eum cilindro de 3l fica por volta de uns 700 eais, o aluguel (esquecid epergutar o periodo) é 50 reais, até ai já maginava esses preços.
Mas me decepcionei quando ele disse que cada carga custa 50 reais, e que num cilindrod e 3l daria pr fazer uns 3 períodos de15 minutos de inalação. Ou seja vi uma graninha se você quiser usar continuamente.

É pra se pensar anyway, de repet compensa.

Deve ser bom dar uma inalada na hora que o cara em um orgasmo, pq é qdo o pulmão puxa mais onigênio imo.

Imaginei o manolão batendo uma punheta com um cilindro do lado e puxando essa merda bem na hora H, meh.

Tipo um velho de 78 anos vendo uns videos?kkkkkk