PAOLO JOSE CESARE BISELLI
Projetos de Pesquisa
Unidades Organizacionais
SCPACIN-62, Hospital Universitário
4 resultados
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- Nasal high-flow therapy reduces work of breathing compared with oxygen during sleep in COPD and smoking controls: a prospective observational study(2017) BISELLI, Paolo J. C.; KIRKNESS, Jason P.; GROTE, Ludger; FRICKE, Kathrin; SCHWARTZ, Alan R.; SMITH, Philip; SCHNEIDER, HartmutPatients with chronic obstructive pulmonary disease (COPD) endure excessive resistive and elastic loads leading to chronic respiratory failure. Oxygen supplementation corrects hypoxemia but is not expected to reduce mechanical loads. Nasal high-flow (NHF) therapy supports breathing by reducing dead space, but it is unclear how it affects mechanical loads of patients with COPD. The objective of this study was to compare the effects of low-flow oxygen and NHF therapy on ventilation and work of breathing (WOB) in patients with COPD and controls during sleep. Patients with COPD (n = 12) and controls (n = 6) were recruited and submitted to polysomnography to measure sleep parameters and ventilation in response to administration of oxygen and NHF. A subset of six patients also had an esophageal catheter inserted for the purpose of measuring WOB. Patients with COPD had similar minute ventilation (V-E) but lower tidal volumes than matched controls. With oxygen, SaO(2) was increased and V-E was reduced in both controls and patients with COPD, but there was an increase in transcutaneous CO2 levels. NHF produced a greater reduction in V-E and was associated with a reduction in CO2 levels. Although NHF halved WOB, oxygen produced only a minor reduction in this parameter. We conclude that oxygen produced little change in WOB, which was associated with CO2 elevations. On the other hand, NHF produced a large reduction in V-E and WOB with a concomitant decrease in CO2 levels. Our data indicate that NHF improves alveolar ventilation during sleep compared with oxygen and room air in patients with COPD and therefore can decrease their cost of breathing. NEW & NOTEWORTHY Nasal high-flow (NHF) therapy can support ventilation in patients with chronic obstructive pulmonary disease during sleep by decreasing the work of breathing and improving CO2 levels. On the other hand, oxygen supplementation corrects hypoxemia, but it produces only a minimal reduction in work of breathing and is associated with increased CO2 levels. Therefore, NHF can be a useful method to assist ventilation in patients with increased respiratory mechanical loads.
- The effect of increased lung volume in chronic obstructive pulmonary disease on upper airway obstruction during sleep(2015) BISELLI, Paolo; GROSSMAN, Peter R.; KIRKNESS, Jason P.; PATIL, Susheel P.; SMITH, Philip L.; SCHWARTZ, Alan R.; SCHNEIDER, HartmutPatients with chronic obstructive pulmonary disease (COPD) exhibit increases in lung volume due to expiratory airflow limitation. Increases in lung volumes may affect upper airway patency and compensatory responses to inspiratory flow limitation (IFL) during sleep. We hypothesized that COPD patients have less collapsible airways inversely proportional to their lung volumes, and that the presence of expiratory airflow limitation limits duty cycle responses to defend ventilation in the presence of IFL. We enrolled 18 COPD patients and 18 controls, matched by age, body mass index, sex, and obstructive sleep apnea disease severity. Sleep studies, including quantitative assessment of airflow at various nasal pressure levels, were conducted to determine upper airway mechanical properties [passive critical closing pressure (Pcrit)] and for quantifying respiratory timing responses to experimentally induced IFL. COPD patients had lower passive Pcrit than their matched controls (COPD: -2.8 +/- 0.9 cmH(2)O; controls: -0.5 +/- 0.5 cmH(2)O, P = 0.03), and there was an inverse relationship of subject's functional residual capacity and passive Pcrit (-1.7 cmH(2)O/l increase in functional residual capacity, r(2) = 0.27, P = 0.002). In response to IFL, inspiratory duty cycle increased more (P = 0.03) in COPD patients (0.40 to 0.54) than in controls (0.41 to 0.51) and led to a marked reduction in expiratory time from 2.5 to 1.5 s (P < 0.01). COPD patients have a less collapsible airway and a greater, not reduced, compensatory timing response during upper airway obstruction. While these timing responses may reduce hypoventilation, it may also increase the risk for developing dynamic hyperinflation due to a marked reduction in expiratory time.
- Lung Mechanics Over the Century: From Bench to Bedside and Back to Bench(2022) BISELLI, Paolo Jose Cesare; LOPES, Fernanda Degobbi Tenorio Quirino Dos Santos; RIGHETTI, Renato Fraga; MORIYA, Henrique Takachi; TIBERIO, Iolanda Ftima Lopes Calvo; MARTINS, Milton ArrudaLung physiology research advanced significantly over the last 100 years. Respiratory mechanics applied to animal models of lung disease extended the knowledge of the workings of respiratory system. In human research, a better understanding of respiratory mechanics has contributed to development of mechanical ventilators. In this review, we explore the use of respiratory mechanics in basic science to investigate asthma and chronic obstructive pulmonary disease (COPD). We also discuss the use of lung mechanics in clinical care and its role on the development of modern mechanical ventilators. Additionally, we analyse some bench-developed technologies that are not in widespread use in the present but can become part of the clinical arsenal in the future. Finally, we explore some of the difficult questions that intensive care doctors still face when managing respiratory failure. Bringing back these questions to bench can help to solve them. Interaction between basic and translational science and human subject investigation can be very rewarding, as in the conceptualization of ""Lung Protective Ventilation"" principles. We expect this interaction to expand further generating new treatments and managing strategies for patients with respiratory disease.
- Leptin and the control of pharyngeal patency during sleep in severe obesity(2014) SHAPIRO, Steven D.; CHIN, Chien-Hung; KIRKNESS, Jason P.; MCGINLEY, Brian M.; PATIL, Susheel P.; POLOTSKY, Vsevolod Y.; BISELLI, Paolo Jose Cesare; SMITH, Philip L.; SCHNEIDER, Hartmut; SCHWARTZ, Alan R.Rationale: Obesity imposes mechanical loads on the upper airway, resulting in flow limitation and obstructive sleep apnea (OSA). In previous animal models, leptin has been considered to serve as a stimulant of ventilation and may prevent respiratory depression during sleep. We hypothesized that variations in leptin concentration among similarly obese individuals will predict differences in compensatory responses to upper airway obstruction during sleep. Methods: An observational study was conducted in 23 obese women [body mass index (BMI): 46 +/- 3 kg/m(2), age: 41 +/- 12 yr] and 3 obese men (BMI: 46 +/- 3 kg/m(2), age: 43 +/- 4 yr). Subjects who were candidates for bariatric surgery were recruited to determine upper airway collapsibility under hypotonic conditions [pharyngeal critical pressure (passive PCRIT)], active neuromuscular responses to upper airway obstruction during sleep, and overnight fasting serum leptin levels. Compensatory responses were defined as the differences in peak inspiratory airflow (Delta V(I)max), inspired minute ventilation (Delta V-I), and pharyngeal critical pressure (Delta P-CRIT) between the active and passive conditions. Results: Leptin concentration was not associated with sleep disordered breathing severity, passive P-CRIT, or baseline ventilation. In the women, increases in serum leptin concentrations were significantly associated with increases in Delta V(I)max (r(2) = 0.44, P < 0.001), Delta V-I (r(2) = 0.40, P < 0.001), and Delta P-CRIT (r(2) = 0.19, P < 0.04). These responses were independent of BMI, waist-to-hip ratio, neck circumference, or sagittal girth. Conclusion: Leptin may augment neural compensatory mechanisms in response to upper airway obstruction, minimizing upper airway collapse, and/or mitigating potential OSA severity. Variability in leptin concentration among similarly obese individuals may contribute to differences in OSA susceptibility.