Influence of noninvasive positive pressure ventilation in obese subjects

Dept of Internal Medicine, Schlafmedizinisches Labor, Medizinische Poliklinik, Philipps-University, Marburg, Germany.
European Respiratory Journal (Impact Factor: 7.64). 12/1997; 10(12):2847-52. DOI: 10.1183/09031936.97.10122847
Source: PubMed


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.

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    • "The role of diaphragmatic weakness in the pathogenesis of this disorder remains uncertain, because patients with OHS can generate similar transdiaphragmatic pressures at any level of diaphragmatic activation compared to eucapnic obese subjects [116,117]. Pankow et al. have shown that non-invasive positive-pressure ventilation unloads the inspiratory muscles in patients with OHS [113]. These results emphasize the role of respiratory muscle fatigue in OHS [118,119]. "
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    ABSTRACT: The overlap syndrome of obstructive sleep apnoea (OSA) and chronic obstructive pulmonary disease (COPD), in addition to obesity hypoventilation syndrome, represents growing health concerns, owing to the worldwide COPD and obesity epidemics and related co-morbidities. These disorders constitute the end points of a spectrum with distinct yet interrelated mechanisms that lead to a considerable health burden. The coexistence OSA and COPD seems to occur by chance, but the combination can contribute to worsened symptoms and oxygen desaturation at night, leading to disrupted sleep architecture and decreased sleep quality. Alveolar hypoventilation, ventilation-perfusion mismatch and intermittent hypercapnic events resulting from apneas and hypopneas contribute to the final clinical picture, which is quite different from the “usual” COPD. Obesity hypoventilation has emerged as a relatively common cause of chronic hypercapnic respiratory failure. Its pathophysiology results from complex interactions, among which are respiratory mechanics, ventilatory control, sleep-disordered breathing and neurohormonal disturbances, such as leptin resistance, each of which contributes to varying degrees in individual patients to the development of obesity hypoventilation. This respiratory embarrassment takes place when compensatory mechanisms like increased drive cannot be maintained or become overwhelmed. Although a unifying concept for the pathogenesis of both disorders is lacking, it seems that these patients are in a vicious cycle. This review outlines the major pathophysiological mechanisms believed to contribute to the development of these specific clinical entities. Knowledge of shared mechanisms in the overlap syndrome and obesity hypoventilation may help to identify these patients and guide therapy.
    Respiratory research 11/2013; 14(1):132. DOI:10.1186/1465-9921-14-132 · 3.09 Impact Factor
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    • "Acute hypercapnia may occur in OHS patients independent of loading, for example, in the subset who retain CO2 as a result of excessive oxygen administration or narcotics. In these situations, PPV could diminish both the OSA that inevitably accompanies this form of acute on chronic hypercapnia and unload inspiration [33]. PPV might also provide mandatory backup ventilation until normal ventilatory drive returns. "
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    ABSTRACT: Obesity is increasing world-wide; obesity hypoventilation syndrome (OHS), formerly Pickwickian syndrome, has increased in parallel. Despite its prevalence, OHS has not been studied well, but there is abundant evidence that it is tightly linked with sleep-disordered breathing, most commonly obstructive sleep apnea. This article reviews the pathophysiology of OHS as well as the literature regarding the benefits of treating this disorder with positive airway pressure. We also emphasize that while positive pressure treatments may temporize cardiopulmonary disease progression, simultaneous pursuit of weight reduction is central to long-term management of this condition.
    Pulmonary Medicine 10/2012; 2012:568690. DOI:10.1155/2012/568690
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    • "However, it should be avoided in patients with severe hypotension or life-threatening arrhythmia, and in those who require an endotracheal tube to protect the airways (coma, impaired swallowing, etc; Table 1). Patients who have refractory hypoxaemia [arterial partial oxygen tension (PaO2)/fractional inspired oxygen (FiO2) ≤60], morbid obesity (>200% of ideal body weight) or with unstable angina or acute myocardial infarction should be closely managed by experienced personnel [5,19]. Criteria for NPPV discontinuation and endotracheal intubation must be thoroughly taken into account in order to avoid dangerous delays (Table 2). "
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    ABSTRACT: Our current state of knowledge on noninvasive positive pressure ventilation (NPPV) and technical aspects are discussed in the present review. In patients with chronic obstructive pulmonary disease, NPPV can be considered a valid therapeutic option to prevent endotracheal intubation. Evidence suggests that, before eventual endotracheal intubation, NPPV should be considered as first-line intervention in the early phases of acute exacerbation of chronic obstructive pulmonary disease. Small randomized and non-randomized studies on the application of NPPV in patients with acute hypoxaemic respiratory failure showed promising results, with reduction in complications such as sinusitis and ventilator-associated pneumonia, and in the duration of intensive care unit stay. The conventional use of NPPV in hypoxaemic acute respiratory failure still remains controversial, however. Large randomized studies are still needed before extensive clinical application in this condition.
    Critical Care 02/2000; 4(1):15-22. DOI:10.1186/cc645 · 4.48 Impact Factor
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