Article

Influence of noninvasive positive pressure ventilation on inspiratory muscle activity in obese subjects.

Dept of Internal Medicine, Schlafmedizinisches Labor, Medizinische Poliklinik, Philipps-University, Marburg, Germany.
European Respiratory Journal (Impact Factor: 7.13). 12/1997; 10(12):2847-52. DOI: 10.1183/09031936.97.10122847
Source: PubMed

ABSTRACT Noninvasive positive pressure ventilation (NPPV) can improve ventilation in obese subjects during the postoperative period after abdominal surgery. Compared to nasal continuous positive airway pressure (nCPAP), NPPV was superior in correcting blood gas abnormalities both during the night-time and during the daytime in a subgroup of patients with the obesity hypoventilation syndrome (OHS). However, as it is unknown, if and to what extent NPPV can unload the respiratory muscles in the face of the increased impedance of the respiratory system in obesity, this is what was investigated. Eighteen obese subjects with a body mass index > or = 40 kg x m(-2) were investigated during the daytime, which included five healthy controls (simple obesity (SO)), seven patients with obstructive sleep apnoea (OSA) and six patients with the obesity hypoventilation syndrome (OHS). Assisted PPV was performed with bi-level positive airway pressure (BiPAP), applied via a face mask. Inspiratory positive airway pressure (IPAP) was set to 1.2 or 1.6 kPa and expiratory positive airway pressure (EPAP) was set to 0.5 kPa. Inspiratory muscle activity was measured as diaphragmatic pressure time product (PTPdi). Comparison of spontaneous breathing with BiPAP ventilation showed no significant difference in breathing pattern, although there was a tendency towards an increase in tidal volume (VT) in all three groups and a decrease in respiratory frequency (fR) in patients with OSA and OHS. End-tidal carbon dioxide (PET,CO2) with BiPAP was unchanged in SO and OSA, but was decreased in OHS. In contrast, inspiratory muscle activity was reduced by at least 40% in each group. This was indicated by a decrease in PTPdi with BiPAP 1.2/0.5 kPa from mean+/-SD 39+/-5 to 20+/-9 kPa x s (p<0.05) in SO, from 42+/-7 to 21+/-8 kPa x s (p<0.05) in OSA, and from 64+/-20 to 38+/-17 kPa x s (p<0.05) in OHS. With BiPAP 1.6/0.5 kPa, PTPdi was further reduced to 17+/-6 kPa x s in SO, and to 17+/-6 kPa x s in OSA, but not in OHS (40+/-22 kPa x s). We conclude that noninvasive assisted ventilation unloads the inspiratory muscles in patients with gross obesity.

0 Bookmarks
 · 
58 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: In patients with impaired inspiratory muscle function or altered respiratory system mechanics, an imbalance between load and capacity can arise. The ventilatory control system normally compensates for this by increasing drive to maintain adequate alveolar ventilation levels, thereby keeping arterial CO2 within its normal range. To reduce work of breathing, a pattern of reduced tidal volume and increased respiratory rate occurs. This pattern itself may eventually reduce effective ventilation by increasing dead space ventilation. However, the impact of sleep on breathing and its role in the development of diurnal respiratory failure is often overlooked in this process. Sleep not only reduces respiratory drive, but also diminishes chemoresponsiveness to hypoxia and hypercapnia creating an environment where significant alterations in oxygenation and CO2 can occur. Acute increases in CO2 load especially during rapid eye movement sleep can initiate the process of bicarbonate retention which further depresses ventilatory responsiveness to CO2. Treatment of hypoventilation needs to be directed toward factors underlying its development. Nocturnal noninvasive positive pressure therapy is the most widely used and reliable strategy currently available to manage hypoventilation syndromes. Although this may not consistently alter respiratory muscle strength or the mechanical properties of the respiratory system, it does appear to reset chemosensitivity by reducing bicarbonate, resulting in a more appropriate ventilatory response to CO2 during wakefulness. Not only is diurnal hypoventilation reduced with noninvasive ventilation, but quality of life, functional capacity and survival are also improved. However, close attention to how therapy is set up and used are key factors in achieving clinical benefits. © 2014 American Physiological Society. Compr Physiol 4: 1639-1676, 2014.
    Comprehensive Physiology. 10/2014; 4(4):1639-76.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In the Western world, the prevalence of obese patients in intensive care units (ICU) is increasing. Additionally, morbid obesity has dramatic consequences on pulmonary function [1]. Therefore, respiratory physicians and intensivists are more likely to manage a larger number of acute hypercapnic respiratory failure (AHRF) episodes in patients with a body mass index (BMI) .30 kg?m -2 . Cor pulmonale is a major cause of ICU admission, which requires mechanical ventilation with higher mortality in obese compared with nonobese patients [2]. It is, therefore, surprising that experience of AHRF in obese patients has rarely been reported in the literature and, consequently, evidence-based guidelines remain to be established [3]. If there are very few data in the literature about noninvasive ventilation (NIV) in obese patients with hypoxaemic respiratory failure [4], there are cumulating reports that suggest that NIV plays a key role in the treatment of obese patients with AHRF [5]. AHRF in obese patients: epidemiological data Clinical characteristics and specificities of obese patients hospitalised in ICUs are currently not well established. In a retrospective cohort study in obese and nonobese patients, it has been shown that obese patients had more major comorbidities than nonobese patients, with a higher prevalence of COPD, sleep respiratory disorders, cor pulmonale and pulmonary hypertension [2]. Similarly, obese patients had a higher prevalence of coronary heart diseases and systemic hypertension. In this study, it has been highlighted that pneumonia and hypoxaemic acute respiratory failure were the most frequent hospitalisation reasons for obese patients in the ICU [2]. Although both cohorts had the same severity at admission, mean length of hospital stay was longer in obese patients compared with nonobese patients. This more-prolonged stay was associated with a higher incidence of complications during ICU stay and a more prolonged weaning period [6]. A total of 12% of obese patients were tracheostomised compared with only 4% in nonobese patients. KOENIG [7] found that the probability of inhalation pneumonia was increased in obese patients, especially during post-surgery, due to an increase in abdominal pressure, increased incidence of gastro-oesophageal reflux and an augmented gastric pH. This should be paralleled with physiopathological consequences of obesity with an increased respiratory work during weaning, due to increased airway resistance, a low thoracic Eur Respir Mon, 2008, 41, 47–59. Printed in UK -all rights reserved. Copyright ERS Journals Ltd 2008; European Respiratory Monograph; ISSN 1025-448x.
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Rationale: Among morbidly obese individuals, obstructive sleep apnea (OSA) is highly prevalent with up to 20% suffering from hypoventilation syndrome. An increased diurnal PaCO2, the signature of obesity hypoventilation syndrome (OHS), implies diminished global ventilation, hence the term hypoventilation. Objectives: We hypothesized that hypercapnic OSA patients have lower minute ventilation than eucapnic OSA patients. Methods and Measurements: In this prospective study we recorded respiratory variables to determine the pathophysiological mechanisms of steady state diurnal hypercapnia of 12 consecutive hypercapnic and 20 consecutive eucapnic OSA patients, matched for apnea hypopnea index. Patients with any known causes of hypercapnia were not included. Results: Comparing hypercapnic to eucapnic patients, the mean values (± SD) for PaCO2 (52±5 vs. 40±3 mm Hg) was significantly higher and the mean PaO2 (59±8 vs. 75±10 mm Hg) was significantly lower in the hypercapnic patients. Surprisingly, the mean values for minute ventilation (12.2±3.0 vs.11.6±2.0 l/minute), alveolar ventilation, breathing rate, tidal volume and dead space did not differ significantly. However, hypercapnic patients had a significantly greater CO2 production (336±79 vs. 278±58 ml/minute) which was the main reason for hypercapnia. When adjusted for body surface area, the mean values for CO2 production were similar between the two groups. Conclusions: These data emphasize the importance of weight loss which could potentially reverse hypercapnic OSA to eucapnic OSA, hypothetically even in the absence of improvement in apnea hypopnea index. In addition, reversal of hypercapnia should also improve oxygenation, both during sleep and while awake, minimizing hypoxia-induced organ dysfunction of OHS.
    Annals of the American Thoracic Society. 05/2014;

Preview

Download
0 Downloads
Available from