Obesity hypoventilation syndrome describes the association between obesity and the development of chronic daytime alveolar hypoventilation. This syndrome arises from a complex interaction between sleep-disordered breathing, diminished respiratory drive, and obesity-related respiratory impairment, and is associated with significant morbidity and mortality. Therapy directed toward reversing these abnormalities leads to improved daytime breathing, with available treatment options including positive pressure therapy, weight loss, and pharmacological management. However, a lack of large-scale, well-designed studies evaluating these various therapies has limited the development of evidence-based treatment recommendations. Although treatment directed toward improving sleep-disordered breathing is usually effective, not all patients tolerate mask ventilation and awake hypercapnia may persist despite effective use. In the longer term, weight loss is desirable, but data on the success and sustainability of this app...

Obesity Hypoventilation Syndrome

Obesity hypoventilation syndrome (OHS) is defined as hypercapnia ­during wakefulness in an obese patient, without any other known cause, accompanied with some form of sleep-disordered breathing as reported by Mokhlesi et al. (Proc Am Thorac Soc 5:218–25, 2008). Although the effects of OHS are inadequately studied, available data show that morbidity and mortality are high. Among those with obstructive sleep apnea (OSA), risk factors for having OHS include a higher body mass index (BMI), an increased severity of sleep-disordered breathing, and a restrictive defect on pulmonary function testing. While the pathophysiology of the disorder remains unclear, it likely involves the presence of several defects, most notably a blunted central respiratory drive. The most effective treatment option consists of ventilatory support during sleep, in the form of positive airway pressure therapy, with or without supplemental oxygen.

pdf/obesity-hypoventilation-syndrome-uhqolyo63n.pdf

Pulmonary hypertension (PH), defined by increased pressure within the pulmonary vasculature, is a hemodynamic and pathophysiologic state present in a wide variety of cardiovascular, respiratory, and systemic diseases. The purpose of this consensus statement is to provide a multidisciplinary approach to guidelines for the diagnosis, classification, treatment, and monitoring of PH in dogs. Comprehensive evaluation including consideration of signalment, clinical signs, echocardiographic parameters, and results of other diagnostic tests supports the diagnosis of PH and allows identification of associated underlying conditions. Dogs with PH can be classified into the following 6 groups: group 1, pulmonary arterial hypertension; group 2, left heart disease; group 3, respiratory disease/hypoxia; group 4, pulmonary emboli/pulmonary thrombi/pulmonary thromboemboli; group 5, parasitic disease (Dirofilaria and Angiostrongylus); and group 6, disorders that are multifactorial or with unclear mechanisms. The approach to treatment of PH focuses on strategies to decrease the risk of progression, complications, or both, recommendations to target underlying diseases or factors contributing to PH, and PH-specific treatments. Dogs with PH should be monitored for improvement, static condition, or progression, and any identified underlying disorder should be addressed and monitored simultaneously.

/pdf/acvim-consensus-statement-guidelines-for-the-diagnosis-2eh8tayjgd.pdf

ACVIM consensus statement guidelines for the diagnosis, classification, treatment, and monitoring of pulmonary hypertension in dogs

Perioperative management of obstructive sleep apnea in bariatric surgery: a consensus guideline

The development of pulmonary hypertension is a poor prognostic sign in patients with obstructive sleep apnea (OSA) and affects both mortality and quality of life. Although pulmonary hypertension in OSA is traditionally viewed as a result of apneas and intermittent hypoxia during sleep, recent studies indicate that neither of these factors correlates very well with pulmonary artery pressure. Human data show that pulmonary hypertension in the setting of OSA is, in large part, due to left heart dysfunction with either preserved or diminished ejection fraction. Longstanding increased left heart filling pressures eventually lead to pulmonary venous hypertension. The combination of hypoxic pulmonary vasoconstriction and pulmonary venous hypertension with abnormal production of mediators will result in vascular cell proliferation and aberrant vascular remodeling leading to pulmonary hypertension. These changes are in many ways similar to those seen in other forms of pulmonary hypertension and suggest shared mechanisms. The majority of patients with OSA do not receive a diagnosis and are undertreated. Appreciating the high prevalence and understanding the mechanisms of pulmonary hypertension in OSA would lead to better recognition and management of the condition.

https://journals.sagepub.com/doi/pdf/10.1086/679995

Pulmonary hypertension in obstructive sleep apnea: is it clinically significant? A critical analysis of the association and pathophysiology

Pulmonary hypertension in obesity-hypoventilation syndrome.

Introduction: In Obesity-Hypoventilation-Syndrome (OHS), pulmonary hypertension (PH) is considered a common feature. Aims: To determine frequency and severity of PH in OHS patients treated with non-invasive pressure ventilation (NPPV). Methods: Prospective cross-sectional study of consecutive patients admitted for follow-up of NPPV (initiated ≥3 months before). OHS was defined by BMI≥30kg/m 2 , capillary carbondioxid tension (PaCO 2 )≥45mmHg prior NPPV initiation without other causes for hypoventilation. Right-heart catheterization (RHC) was performed at rest without oxygen supplementation, daytime sleepiness measured by Epworth Sleepiness Scale (ESS). Results: 177 patients considered to have OHS were screened. Among 64 patients who met the diagnosis criteria for OHS, 21 patients (10f, 11m; median age 62.2 [53.9;71.7] years, BMI 45 [40;53] kg/m 2 , PaCO 2 39.6 [37.8;45.5] mmHg) gave consent for RHC. Only 4 (19%) patients had normal mean pulmonary artery pressure (mPAP 2 /cm 5 ; 8 patients (38.1%) presented with “Borderline”-PH (mPAP 20-24mmHg), mPAP 22 [22.5;23] mmHg and PVRI 392 [287;485] and 9 patients (42.9%) had a manifest PH (mPAP≥25mmHg), mPAP 33 [29;34] mmHg and PVRI 440 [384;728]. In 3 patients with PH, pulmonary capillary wedge pressure was >15mmHg; 2 of them presented with transpulmonary pressure gradient >12mmHg. In patients with PH, ESS (7 [6;11]) was significantly higher than in those without PH (3 [0.5;5.5], p=0.03) or Borderline-PH (3.5 [2.5;6.5], p=0.03). Conclusion: Mild to moderate PH is quite frequent in OHS, even after initiation of NPPV. Its impact on survival and quality of life has to be studied in future trials.

Pulmonary hypertension in obesity-hypoventilation-syndrome

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Pulmonary hypertension in obesity-hypoventilation syndrome.

Pulmonary hypertension in obesity-hypoventilation-syndrome