Classificação de Mallampati em fonação para predição da dificuldade de intubação traqueal em obesos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influencia da obesidade na correlacao entre refluxo faringolaringeo e apneia obstrutiva do sono

Introdução:A apneia obstrutiva do sono (AOS) é causada por episódios recorrentes de obstrução total ou parcial da via aérea superior com duração superior a 10 segundos durante o sono. Refluxo faringolaríngeo (RFL) é uma variante da doença do refluxo gastroesofágico que afeta a laringe e a faringe.Objetivos:Avaliar a influência da obesidade na relação entre RFL e AOS em pacientes com SAOS.Materiais e métodos:Estudo observacional transversal retrospectivo. Foram revisados protocolos de atendimento de pacientes com AOS que incluem questionários validados para RFL como Reflux Sympton Index (RSI) e Reflux Finding Score (RSI), nasolaringofibroscopia e polissonografia.Resultados:Cento e cinco pacientes foram divididos em grupo de obesos (39 pacientes) e não obesos (66 pacientes). Na avaliação das médias do RSI o grupo de não obesos foi semelhante entre pacientes com AOS leve (11,96) e moderada (11,43). No grupo de obesos a média do RSI foi de 6,7 em pacientes com AOS leve e de 11,53 em pacientes com AOS moderada a grave (p < 0,05).Discussão:O subgrupo de pacientes com AOS e RFL apresenta vários fatores que promovem a inflamação da via aérea superior. Pacientes com AOS devem ser pesquisados e tratados quanto a RFL, aumentando a qualidade de vida.Conclusão:O RFL e a AOS se correlacionam positivamente em pacientes obesos.

A systematic review and meta-analysis of cohort studies of echocardiographic findings in OSA children after adenotonsilectomy

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

The nucleus of the solitary tract and the coordination of respiratory and sympathetic activities

It is well known that breathing introduces rhythmical oscillations in the heart rate and arterial pressure levels. Sympathetic oscillations coupled to the respiratory activity have been suggested as an important homeostatic mechanism optimizing tissue perfusion and blood gas uptake/delivery. This respiratory-sympathetic coupling is strengthened in conditions of blood gas challenges (hypoxia and hypercapnia) as a result of the synchronized activation of brainstem respiratory and sympathetic neurons, culminating with the emergence of entrained cardiovascular and respiratory reflex responses. Studies have proposed that the ventrolateral region of the medulla oblongata is a major site of synaptic interaction between respiratory and sympathetic neurons. However, other brainstem regions also play a relevant role in the patterning of respiratory and sympathetic motor outputs. Recent findings suggest that the neurons of the nucleus of the solitary tract (NTS), in the dorsal medulla, are essential for the processing and coordination of respiratory and sympathetic responses to hypoxia. The NTS is the first synaptic station of the cardiorespiratory afferent inputs, including peripheral chemoreceptors, baroreceptors and pulmonary stretch receptors. The synaptic profile of the NTS neurons receiving the excitatory drive from afferent inputs is complex and involves distinct neurotransmitters, including glutamate, ATP and acetylcholine. In the present review we discuss the role of the NTS circuitry in coordinating sympathetic and respiratory reflex responses. We also analyze the neuroplasticity of NTS neurons and their contribution for the development of cardiorespiratory dysfunctions, as observed in neurogenic hypertension, obstructive sleep apnea and metabolic disorders.

Perfil clínico de crianças com indicação da cirurgia das tonsilas em um hospital terciário universitário

The indications for adenotonsillectomy in pediatric patients have changed considerably during the 90th decade. Local or systemic complications of the adenoid or tonsil hypertrophy itself have now been substituted by signs of obstructive ventilatory disturbances, including obstructive sleep apnea as the major indications for surgery. Objective: This study analyses the clinical profile of children submitted to adenotonsilectomy in their pre and postoperative state, at Botucatu Medical School-State University São Paulo, UNESP. Methods: 332 children of both genders, aged 1 to 12 years, who underwent adenotonsillectomy between 1999 and 2004, were studied, focused on epidemiological profile, pre and postoperative (1 month) symptoms, obtained from medical records. Height and weight were compared to brazilian normal age related values. Results: We found a predominance of the male gender, except in he group aged from 10 to 12 years. Considering wheight and height, we found important failure to thrive, mostly for height deficit. Among clinical aspects, we found a significant reduction in obstructive symptoms like snoring or apneia (p<0001) in the postoperative period. Conclusion: Our results were similar to the literature findings of patients clinical profile. The major indication for adenotonsillectomy in our service was clinical diagnosis of obstructive sleep apnea.

Coupling between respiratory and sympathetic activities as a novel mechanism underpinning neurogenic hypertension

Enhanced sympathetic outflow to the heart and resistance vessels greatly contributes to the onset and maintenance of neurogenic hypertension. There is a consensus that the development of hypertension (clinical and experimental) is associated with an impairment of sympathetic reflex control by arterial baroreceptors. More recently, chronic peripheral chemoreflex activation, as observed in obstructive sleep apnea, has been proposed as another important risk factor for hypertension. In this review, we present and discuss recent experimental evidence showing that changes in the respiratory pattern, elicited by chronic intermittent hypoxia, play a key role in increasing sympathetic activity and arterial pressure in rats. This concept parallels results observed in other models of neurogenic hypertension, such as spontaneously hypertensive rats and rats with angiotensin II–salt-induced hypertension, pointing out alterations in the central coupling of respiratory and sympathetic activities as a novel mechanism underlying the development of neurogenic hypertension.

Dinâmica de grafoelementos do sono e seus impactos na neurofisiologia de pacientes com apneia obstrutiva através de sinais de eletroencefalografia

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Central leptin replacement enhances chemorespiratory responses in leptin-deficient mice independent of changes in body weight

Previous studies showed that leptin-deficient (ob/ob) mice develop obesity and impaired ventilatory responses to CO2 . In this study, we examined if leptin replacement improves chemorespiratory responses to hypercapnia (7 % CO2) in ob/ob mice and if these effects were due to changes in body weight or to the direct effects of leptin in the central nervous system (CNS). was measured via plethysmography in obese leptin-deficient- (ob/ob) and wild-type- (WT) mice before and after leptin (10 mu g/2 mu l day) or vehicle (phosphate buffer solution) were microinjected into the fourth ventricle for four consecutive days. Although baseline was similar between groups, obese ob/ob mice exhibited attenuated compared to WT mice (134 +/- 9 versus 196 +/- 10 ml min(-1)). Fourth ventricle leptin treatment in obese ob/ob mice significantly improved (from 131 +/- 15 to 197 +/- 10 ml min(-1)) by increasing tidal volume (from 0.38 +/- 0.03 to 0.55 +/- 0.02 ml, vehicle and leptin, respectively). Subcutaneous leptin administration at the same dose administered centrally did not change in ob/ob mice. Central leptin treatment in WT had no effect on . Since the fourth ventricle leptin treatment decreased body weight in ob/ob mice, we also examined in lean pair-weighted ob/ob mice and found it to be impaired compared to WT mice. Thus, leptin deficiency, rather than obesity, is the main cause of impaired in ob/ob mice and leptin appears to play an important role in regulating chemorespiratory response by its direct actions on the CNS.

Chronic Intermittent Hypoxia Depresses Afferent Neurotransmission in NTS Neurons by a Reduction in the Number of Active Synapses

Long-term synaptic plasticity has been recently described in brainstem areas associated to visceral afferent sensory integration. Chronic intermittent hypoxia (CIH), an animal model for studying obstructive sleep apnea in humans, depresses the afferent neurotransmission in nucleus tractus solitarii (NTS) neurons, which affect respiratory and autonomic regulation. Here we identified the synaptic mechanisms of CIH-induced depression of the afferent neurotransmission in NTS neurons in juvenile rats. We verified that CIH reduced the amplitude of both NMDA and non-NMDA glutamatergic excitatory currents (eEPSCs) evoked by tractus solitarii stimulation (TS-eEPSC) of second-order neurons in the NTS. No changes were observed in release probability, evidenced by absence of any CIH-elicited effects on short-term depression and failures in EPSCs evoked in low calcium. CIH also produced no changes in TS-eEPSC quantal size, since the amplitudes of both low calcium-evoked EPSCs and asynchronous TS-eEPSCs (evoked in the presence of Sr2+) were unchanged. Using single TS afferent fiber stimulation in slices from control and CIH rats we clearly show that CIH reduced the quantal content of the TS-eEPSCs without affecting the quantal size or release probability, suggesting a reduction in the number of active synapses as the mechanism of CIH induced TS-eEPSC depression. In accordance with this concept, the input-output relationship of stimulus intensity and TS-eEPSC amplitude shows an early saturation in CIH animals. These findings open new perspectives for a better understanding of the mechanisms underlying the synaptic plasticity in the brainstem sensory neurons under challenges such as those produced by CIH in experimental and pathological conditions.

Acute hypoxia induces hypertriglyceridemia by decreasing plasma triglyceride clearance in mice

Jun JC, Shin MK, Yao Q, Bevans-Fonti S, Poole J, Drager LF, Polotsky VY. Acute hypoxia induces hypertriglyceridemia by decreasing plasma triglyceride clearance in mice. Am J Physiol Endocrinol Metab 303: E377-E388, 2012. First published May 22, 2012; doi:10.1152/ajpendo.00641.2011.-Obstructive sleep apnea (OSA) induces intermittent hypoxia (IH) during sleep and is associated with elevated triglycerides (TG). We previously demonstrated that mice exposed to chronic IH develop elevated TG. We now hypothesize that a single exposure to acute hypoxia also increases TG due to the stimulation of free fatty acid (FFA) mobilization from white adipose tissue (WAT), resulting in increased hepatic TG synthesis and secretion. Male C57BL6/J mice were exposed to FiO(2) = 0.21, 0.17, 0.14, 0.10, or 0.07 for 6 h followed by assessment of plasma and liver TG, glucose, FFA, ketones, glycerol, and catecholamines. Hypoxia dose-dependently increased plasma TG, with levels peaking at FiO(2) = 0.07. Hepatic TG levels also increased with hypoxia, peaking at FiO(2) = 0.10. Plasma catecholamines also increased inversely with FiO(2). Plasma ketones, glycerol, and FFA levels were more variable, with different degrees of hypoxia inducing WAT lipolysis and ketosis. FiO(2) = 0.10 exposure stimulated WAT lipolysis but decreased the rate of hepatic TG secretion. This degree of hypoxia rapidly and reversibly delayed TG clearance while decreasing [H-3]triolein-labeled Intralipid uptake in brown adipose tissue and WAT. Hypoxia decreased adipose tissue lipoprotein lipase (LPL) activity in brown adipose tissue and WAT. In addition, hypoxia decreased the transcription of LPL, peroxisome proliferator-activated receptor-gamma, and fatty acid transporter CD36. We conclude that acute hypoxia increases plasma TG due to decreased tissue uptake, not increased hepatic TG secretion.

Chronic intermittent hypoxia alters glutamatergic control of sympathetic and respiratory activities in the commissural NTS of rats

Costa-Silva JH, Zoccal DB, Machado BH. Chronic intermittent hypoxia alters glutamatergic control of sympathetic and respiratory activities in the commissural NTS of rats. Am J Physiol Regul Integr Comp Physiol 302: R785-R793, 2012. First published December 28, 2011; doi:10.1152/ajpregu.00363.2011.-Sympathetic overactivity and altered respiratory control are commonly observed after chronic intermittent hypoxia (CIH) exposure. However, the central mechanisms underlying such neurovegetative dysfunctions remain unclear. Herein, we hypothesized that CIH (6% O-2 every 9 min, 8 h/day, 10 days) in juvenile rats alters glutamatergic transmission in the commissural nucleus tractus solitarius (cNTS), a pivotal site for integration of peripheral chemoreceptor inputs. Using an in situ working heart-brain stem preparation, we found that L-glutamate microinjections (1, 3, and 10 mM) into the cNTS of control rats (n = 8) evoked increases in thoracic sympathetic nerve (tSN) and central vagus nerve (cVN) activities combined with inhibition of phrenic nerve (PN) activity. Besides, the ionotropic glutamatergic receptor antagonism with kynurenic acid (KYN; 250 mM) in the cNTS of control group (n = 7) increased PN burst duration and frequency. In the CIH group (n = 10), the magnitude of L-glutamate-induced cVN excitation was smaller, and the PN inhibitory response was blunted (P < 0.05). In addition, KYN microinjections into the cNTS of CIH rats (n = 9) did not alter PN burst duration and produced smaller increases in its frequency compared with controls. Moreover, KYN microinjections into the cNTS attenuated the sympathoexcitatory response to peripheral chemoreflex activation in control but not in CIH rats (P < 0.05). These functional CIH-induced alterations were accompanied by a significant 10% increase of N-methyl-D-aspartate receptor 1 (NMDAR1) and glutamate receptor 2/3 (GluR2/3) receptor subunit density in the cNTS (n = 3-8, P < 0.05), evaluated by Western blot analysis. These data indicate that glutamatergic transmission is altered in the cNTS of CIH rats and may contribute to the sympathetic and respiratory changes observed in this experimental model.

Analyzing training dependencies and posterior fusion in discriminant classification of apnoea patients based on sustained and connected speech

We present a novel approach using both sustained vowels and connected speech, to detect obstructive sleep apnea (OSA) cases within a homogeneous group of speakers. The proposed scheme is based on state-of-the-art GMM-based classifiers, and acknowledges specifically the way in which acoustic models are trained on standard databases, as well as the complexity of the resulting models and their adaptation to specific data. Our experimental database contains a suitable number of utterances and sustained speech from healthy (i.e control) and OSA Spanish speakers. Finally, a 25.1% relative reduction in classification error is achieved when fusing continuous and sustained speech classifiers. Index Terms: obstructive sleep apnea (OSA), gaussian mixture models (GMMs), background model (BM), classifier fusion.

Análise crítica das técnicas de tratamento cirúrgico da obesidade mórbida

Introdução: A obesidade é uma afecção com alta prevalência no Brasil e no mundo. É fator de risco para comorbidades como Diabetes tipo 2 (DM2), Hipertensão Arterial Sistêmica (HAS), Dislipidemia, Apneia Obstrutiva do Sono (AOS), entre outras. Seu tratamento é complexo e a cirurgia bariátrica, executada por diferentes técnicas, tem sido uma das opções. Objetivo: Analisar os resultados publicados na literatura em relação às técnicas cirúrgicas de Banda Gástrica Ajustável (BGA), Gastrectomia Vertical (GV), Gastroplastia com derivação em Y de Roux (GDYR) e Derivação Biliopancreática (DBP) - técnica de \"Scopinaro\" e de \"Duodenal Switch\" quanto às complicações operatórias, à mortalidade, à perda do excesso de peso (PEP) e ao reganho, e a resolução das comorbidades após a operação. Método: Foram analisados 116 estudos selecionados na base de dados MEDLINE por meio da PubMed publicados na Língua Inglesa entre 2003 e 2014. Para comparar as diferentes técnicas cirúrgicas (BGA, GV, GDYR e DBP), realizou-se estudo estatístico por meio da análise de variância (ANOVA) aplicando os testes de Duncan e de Kruskal Wallis avaliando: complicações pós-operatórias (fístula, sangramento e óbito); perda e reganho do excesso de peso, e resolução das comorbidades. Resultados: A ocorrência de sangramento foi de 0,6% na média entre todos os estudos, sendo 0,44% na BGA; 1,29% na GV; 0,81% na GDYR e 2,09% na DBP. Já a ocorrência de fístulas foi de 1,3% na média entre todos os estudos, 0,68% para BGA; 1,93% para GV; 2,18% para GDYR e 5,23% para DBP. A mortalidade nos primeiros 30 dias pós-operatórios foi de 0,9% na média entre todos os estudos, 0,05% na BGA; 0,16% na GV; 0,60% na GDYR e 2,52% na DBP. A PEP após cinco anos na média entre todos os estudos foi de 63,86%, especificamente na BGA, foi de 48,35%; 52,7% na GV; 71,04% na GDYR e 77,90% na DBP. A taxa de DM2 resolvida foi de 76,9% na média entre todos os estudos, sendo 46,80% na BGA; 79,38% na GV; 79,86% na GDYR e 90,78% na DBP. A taxa de Dislipidemia resolvida após a operação foi de 74,0% na média de todo o estudo, sendo 51,28% na BGA; 58,00% na GV; 73,28% na GDYR e 90,75% na DBP. A taxa de HAS resolvida após a operação foi de 61,80% na média de todo o estudo, sendo 54,50% na BGA; 52,27% na GV; 68,11% na GDYR e 82,12% na DBP. A taxa de AOS resolvida após a operação foi de 75,0% na média de todo o estudo, sendo 56,85% na BGA; 51,43% na GV; 80,31% na GDYR e 92,50% na DBP. Conclusão: quando analisadas e comparada as quatro técnicas observa-se que nos primeiros 30 dias pós-operatório a taxa de sangramento é superior nos pacientes submetidos à DBP e taxa de fístula inferior nos pacientes da BGA. Quanto à mortalidade observou-se taxa mais pronunciada nos pacientes submetidos à DBP e menos nos submetidos à BGA. Quanto à PEP observou-se uma uniformidade entre os pacientes submetidos à GV, GDYR E DBP até o terceiro ano. Após esse período observa-se reganho de peso nos submetidos à GV até o quinto ano de seguimento. Já nos pacientes submetidos à BGA observou-se taxas de PEP menos pronunciadas em relação às demais desde o início do seguimento. Quanto à resolução das comorbidades observou-se taxas de resolução de DM2 inferiores nos pacientes submetidos à BGA, e não houve diferença entre nenhuma técnica quanto à resolução das demais comorbidades: HAS, AOS e dislipidemia

Snoring and its association with asthma in Indigenous children living in the Torres Strait and Northern Peninsula Area

Objective: Respiratory health of Indigenous and minority ethnic groups in affluent countries is poorer than their non-minority counterparts and sleep disorders are no exception. In children, obstructive sleep apnoea has the potential to result in serious long-term consequences. In 1999, we studied 1650 children and adolescents living in the Torres Strait and the Northern Peninsula Area, Australia. Here we report prevalence of snoring in these communities and relate its association with asthma symptoms. Methods: A population-based cross-sectional study was conducted in the Torres Strait region. Five indigenous communities were randomly selected and information was collected using a structured face-to-face interview based on a standardized questionnaire. There was a 98% response rate, and 1650 children, 0-17 years of age, were included in the study. Results: Overall, the prevalence of snoring was 14.2% (95% CI 12.5-15.9); 3.6% (95% CI 2.7-4.6) reported snorting, and 6% (95% CI 4.9-7.2) reported restless sleep. The prevalence of snoring was significantly higher among males (17.1% for males and 10.8 for females, P = 0.005). Children were five times more likely to have experienced snoring and snorting if they reported wheezing in the last 12 months. Conclusion: We conclude that the prevalence of symptoms suggestive of obstructive sleep problems is relatively high in children of this region. This highlights the need for awareness among the community patients and physicians about the problem of obstructive sleep-disordered breathing, especially in children with asthma, and for the need for further studies to measure prevalence of sleep breathing disorders among Indigenous Australians.

Association of subclinical right ventricular dysfunction with obesity

OBJECTIVES The purpose of this research was to identify the determinants of right ventricular (RV) dysfunction in overweight and obese subjects. BACKGROUND Right ventricular dysfunction in obese subjects is usually ascribed to comorbid diseases, especially obstructive sleep apnea. We used tissue Doppler imaging to identify the determinants of RV dysfunction in overweight and obese subjects. METHODS Standard and tissue Doppler echocardiography was performed in 112 overweight (body mass index [BMI] 25 to 29.9 kg/m(2)) or obese (BMI >30 kg/m(1)) subjects and 36 referents (BMI 35 kg/m(2) had reduced RV function compared with referent subjects, evidenced by reduced s(m) (6.5 +/- 2.4 cm/s vs. 10.2 +/- 1.5 cm/s, p < 0.001), peak strain (-21 +/- 4% vs. -28 +/- 4%, p < 0.001), peak strain rate (-1.4 +/- 0.4 s(-1) vs. -2.0 +/- 0.5 s(-1), p < 0.001), and e(m) (6.8 +/- 2.4 cm/s vs. -10.3 +/- 2.5 cm/s, p < 0.001), irrespective of the presence of sleep apnea. Similar but lesser degrees of reduced systolic function (p < 0.05) were present in overweight (BMI 25 to 29.9 kg/m(2)) and mildly obese (BMI 30 to 35 kg/m(2)) groups. Differences in RV e(m), s(m), and strain indexes were demonstrated between the severely versus overweight and mildly obese groups (p < 0.05). Body mass index remained independently related to RV changes after adjusting for age, log insulin, and mean arterial pressures. In obese patients, these changes were associated with reduced exercise capacity but not the duration of obesity and presence of sleep apnea or its severity. CONCLUSIONS Increasing BMI is associated with increasing severity of RV dysfunction in overweight and obese subjects without overt heart disease, independent of sleep apnea.