肺胞低換気症候群

Postoperative respiratory depression (PORD) and other postoperative pulmonary complications (PPCs) represent significant contributors to perioperative morbidity and mortality in companion animal practice. The Confidential Enquiry into Perioperative Small Animal Fatalities (CEPSAF) established that cardiovascular and respiratory causes account for approximately 74% and 72% of perioperative deaths in dogs and cats, respectively, with 47% of canine and 61% of feline anesthetic-related deaths occurring in the postoperative period. PORD arises from a convergence of opioid-induced respiratory depression (OIRD), residual inhalant anesthetic effects, other drug-induced effects (e.g., neuromuscular blockade), and patient-specific vulnerabilities. PPCs encompass a broad spectrum of conditions, including atelectasis, aspiration pneumonia, pneumonia, hypoventilation, acute respiratory distress syndrome (ARDS), and respiratory arrest, with laparotomy studies reporting a PPC incidence of 22% in dogs. This narrative review synthesizes current evidence on the pathophysiology, risk factors, diagnostic approaches, prevention strategies, and treatment of PORD and PPCs in veterinary practice, incorporating insights from both veterinary-specific and translational human anesthesia literature, while explicitly identifying areas where veterinary-specific evidence remains limited. The importance of continuous monitoring during the postanesthetic period, multimodal analgesia to reduce opioid exposure, protective lung ventilation strategies, and early intervention is highlighted as a key strategy to improve outcomes, together with the unmet need for reversal-independent ("agnostic") respiratory stimulants capable of countering PORD irrespective of the causative agent.

BACKGROUND: Optimal long-term management and inspiratory support requirements remain debated in obesity hypoventilation syndrome (OHS). OBJECTIVES: This prospective, observational study assessed inspiratory support requirements in OHS patients initiating noninvasive ventilation (NIV) after acute hypercapnic respiratory failure, using a volume-assured mode targeting normocapnia. METHODS: Ventilator data and clinical parameters were collected at baseline, 1 month, 3 months, 6 months and 12 months after initiation of NIV. Inspiratory support requirements were assessed using driving pressure and apparent respiratory system compliance and compared over time using the Wilcoxon test and Friedman analysis of variance. Groups with persistent and minimal inspiratory support needs at 1 year were compared using Mann-Whitney, χ2 and Cochran Q tests. RESULTS: Of 40 enrolled patients, 39 completed the study. Therapeutic adherence (37 (94.9%)) and efficacy (35 (89.7%)) were high. Inspiratory support requirements decreased over the study period (12.1 (9.6-14.9) to 9.9 (6.3-12.2) cmH₂O, p<0.001), though 84.6% of patients still required >5 cmH₂O driving pressure. Initial driving pressure, higher minute ventilation and higher apparent respiratory system compliance were associated with reduced support requirements after 1 year, but no baseline parameter reliably predicted minimal support need. Reduced ventilatory support at 6 months demonstrated the strongest correlation with maintaining lower driving pressure at 12 months. CONCLUSIONS: Inspiratory support needs reduce over 12 months in OHS patients acutely initiated on long-term NIV, but few patients showed only minimal inspiratory support requirements to maintain normocapnia. Reliable reduction was apparent after 6 months of treatment, suggesting that respiratory muscle recovery is slower than previously assumed. Further studies are needed to verify whether an initial 'hit hard' approach with sequential de-escalation of ventilatory support results in optimal outcome.

Pediatric asthma remains a leading cause of emergency department visits and hospitalizations worldwide. Patients with critical asthma represents a subset of patients requiring respiratory support beyond standard pharmacologic therapy. Management of respiratory support in these patients has evolved dramatically, with intubation rates decreasing from 6.9% to 3.4% between 2009 and 2019 while noninvasive ventilation use doubled and high-flow nasal cannula utilization increased from 11% to 52%. This narrative review examines current evidence and practical considerations for respiratory support strategies across the spectrum of pediatric critical asthma care. The pathophysiology of critical asthma creates unique challenges fundamentally different from other causes of respiratory failure. Dynamic hyperinflation from progressive air trapping and intrinsic positive end-expiratory pressure (PEEP) development represents the cornerstone derangement, requiring ventilation strategies that seems divergent from those utilized in acute respiratory distress syndrome. High-flow nasal cannula provides benefit primarily through dead space washout and gas conditioning, while noninvasive ventilation offers comprehensive support by augmenting ventilation and offsetting intrinsic PEEP effects. When mechanical ventilation becomes necessary, controlled hypoventilation with acceptance of hypercapnia while maintaining pH > 7.20 has dramatically reduced mortality compared with historical approaches targeting normocapnia. Pressure-controlled ventilation may offer physiologic advantages over volume-controlled modes by providing more uniform gas distribution in airways with varying degrees of obstruction. A structured three-phase ventilation approach emphasizes initial hyperinflation clearance, followed by acidosis resolution, then careful weaning with attention to dynamic hyperinflation monitoring. Current survival rates exceed 96% for children reaching medical care, representing substantial improvement from historical mortality rates of 20-30%. Optimal respiratory support in critical asthma requires understanding that mechanical ventilation strategies in asthma differs from other respiratory failure etiologies, with dynamic hyperinflation management taking precedence over traditional lung-protective strategies. Future research priorities include developing severity prediction tools, optimizing noninvasive protocols, and investigating personalized approaches on the basis of emerging understanding of asthma phenotypes and endotypes.

AIM: To explore factors influencing compliance with Non-invasive Positive Pressure Ventilation therapy in patients with obesity hypoventilation syndrome (OHS) prior to bariatric surgery, and to identify enabling factors and barriers using the capability, opportunity, and motivation-behavior model (COM-B model). DESIGN: A qualitative descriptive design. METHODS: Using purposive sampling, 13 patients with OHS who underwent bariatric metabolic surgery in the general surgery department of a tertiary hospital in Taiyuan from March to September 2025 were selected. Face-to-face semi-structured in-depth interviews were conducted, and the interview data underwent content analysis to extract themes. RESULTS: This study summarizes from three main factors: capability, opportunity, and motivation, and extracts the three major facilitating factors and barrier factors for patients with OHS to use Non-invasive Positive Pressure Ventilation (NIPPV) before weight loss surgery. Among them, facilitating factors include: Capability factors (positive perceptions and internalization of health awareness for positive pressure ventilation), Opportunity factors (family support, motivational effects of and peer support, assistance and supervision from professionals), and Motivation factors (urgency of ensuring surgical safety, strong motivation for rehabilitation, fear of severe health consequences, positive feedback from symptom improvement). Barrier factors include: Capability factors (the physiological burden of obese patients, lack of self-efficacy in changing past habits, insufficient cognitive ability), Opportunity factors (insufficient professional support, unfavorable rehabilitation environment), Motivation factors (uncomfortable wearing experience, fatigue while wearing, anxious mind and sense of shame). CONCLUSION: The use of NIPPV before weight loss surgery in patients with OHS is influenced by their capability, opportunity, and motivation. Patients with OHS are highly reliant on authoritative information. Clinical medical staff can leverage "peer support", focus on the spontaneous motivational role of positive pressure ventilation in patients with OHS, and use positive feedback incentive mechanisms to improve the enthusiasm and compliance with positive pressure ventilation, thereby helping patients with OHS achieve better ventilation outcomes. PRACTICE IMPLICATIONS: Clinical interventions should target the above multidimensional factors, focusing on strengthening patient cognitive education and self-efficacy, optimizing family and social support systems, improving wearing comfort, and alleviating psychological burden, thereby effectively enhancing preoperative adherence to NIPPV.

RATIONALE: There is no effective pharmacotherapy for obesity hypoventilation syndrome (OHS). Intranasal leptin augments the hypercapnic ventilatory response (HCVR), attenuates upper airway obstruction, and increases ventilation during sleep in diet-induced obese (DIO) mice. Respiratory effects of leptin can be attenuated by serotonergic antagonists. OBJECTIVES: To establish if serotonergic innervation of the hypoglossal motoneurons (XII MN) mediates effects of leptin on OHS. METHODS: We examined effects of intranasal leptin on the HCVR, sleep architecture, arousal latency, flow limited (obstructed) and non-flow limited breathing, genioglossus muscle (GG) activity and metabolic rate across sleep/wake states in the presence and absence of serotonergic neurons innervating XII MN in DIO Sert-flp mice expressing FlpO recombinase in the serotonergic neurons. These mice were transfected into the XII MN with retrograde adeno-associated virus carrying either FlpO-dependent caspase or control yellow fluorescent protein (YFP). MEASUREMENTS AND MAIN RESULTS: Control YFP virus was densely localized to the serotonergic neurons of the medullary raphe (MR), but not the dorsal raphe (DR), and these neurons were ablated by caspase. Leptin enhanced the HCVR, increased arousal latency in males, but not in females, and these effects were abolished by caspase. Neither leptin nor caspase affected sleep architecture or metabolic rate. Leptin increased GG activity awake and during NREM sleep, attenuated pharyngeal obstruction and increased minute ventilation in NREM and REM sleep. All effects of leptin were abolished by the FlpO-dependent caspase. CONCLUSIONS: Leptin treats OHS by stimulating MR serotonergic neurons, which project to XII MN and stimulate pharyngeal muscles during sleep.