Abstract 1: Obstructive sleep apnea
Professor William Ward Flemons is a professor of medicine at the University of Calgary, in Alberta, Canada. He currently practices respiratory medicine at the Tom Baker Cancer Centre and at Foothills Hospital. He completed fellowships in internal medicine and in respiratory medicine and obtained certifications by the American College of Physicians, and the Royal College of Physicians of Canada. He was the recipient of many distinguished awards throughout his career from different scientific and medical bodies. In addition to academic teaching activities, Prof. Flemons has been a chairperson and an invited speaker in many scientific meetings and public forums. He holds many senior positions in health care facilities as well as in various clinical and educational regional bodies. Prof. Flemons has published numerous original research papers and review articles. His research interest is related to respiratory medicine and quality and safety of health care services.
Abstract 1: Obstructive sleep apnea
Patients with obstructive sleep apnea (OSA) have recurrent brief periods of breathing cessation (apnea) or reduction in tidal volume (hypopnea) during sleep caused by collapse of the upper airway (UAW). OSA often leads to daytime somnolence and reduced quality of life. It affects at least 4% of men and 2% of women; prevalence correlates with BMI and a history of snoring. OSA affects > 50% of severely obese (BMI > 40) patients. It has been causally linked to hypertension (independent of its interaction with obesity), increases the risk of the metabolic syndrome and predisposes some patients to stroke and myocardial infarction. Treatment (continuous positive airway pressure), pneumatically splints open the UAW, is highly effective and available. Long-term compliance with therapy is 50 to 70%. Sleep hypoventilation (SHV) can be seen in severe OSA patients who most often have an excessive BMI; 20% of severely obese OSA patients have SHV. It can also occur in patients with restrictive chest wall disorders or neuromuscular disease. SHV is characterized by hypercarbia that worsens during sleep, most severely during REM sleep when control of breathing (COB) is most precarious. The very severe hypoxemia that occurs during sleep predisposes patients to corpulmonale. SHV occurs because of a complex interplay of factors including upper airway instability, excessive respiratory load, and abnormal COB. Leptin, a protein hormone produced by adipose cells whose function is to act centrally to suppress appetite, may also contribute to reduced central respiratory drive. Treatment with bi-level positive airway pressure (BLPAP) maintains a patent UAW and assisted ventilation because of the pressure difference between the inspiratory and expiratory cycle. Most often BLPAP is effective at controlling and often reversing) corpulmonale and respiratory failure.
Abstract 2: Hypoventilation
Sleep (particularly REM) leads to a resetting of the carbon dioxide (CO2) set-point such that mild hypercarbia (3 - 4 mmHg) normally occurs. When CO2 retention becomes excessive, patients have sleep hypoventilation (SHV); this occurs most commonly in severely obese patients whose body mass index (BMI) exceeds 40 but can also occur in patients with restrictive chest wall disorders, neuromuscular disease or severe obstructive sleep apnea (OSA). Narcotics and benzodiazepines exacerbate SHV. SHV develops due to a complex interplay of factors affecting respiration including central control of breathing (COB), an unstable upper airway that causes increased airflow resistance and abnormal respiratory mechanics; the latter two lead to an increased work of breathing. Diagnosis relies on polysomnography (PSG), a test which records physiologic (breathing rate, airflow, oxygen saturation, respiratory effort, transcutaneous CO2) and electrical (EEG, EMG, EKG) signals. It is supervised overnight by an experienced technologist with detailed scoring and analysis required following the study. OSA is characterized by recurrent brief periods of breathing cessation (apnea) or reduction in tidal volume (hypopnea) during sleep caused by collapse of the upper airway (UAW). The apnea-hypopnea index (AHI) reflects the average number of apneas and hypopneas that occur per hour of sleep. Consensus guidelines characterize severe OSA as an AHI > 30 but some patients’ AHIs exceed 100. PSG is also used to diagnose OSA; however because OSA is highly prevalent and PSG is, in most countries, a limited resource, there can be excessive waits and delays for patients. Therefore, increasingly clinical prediction rules and ambulatory monitoring are being used to diagnose and manage patients with OSA. This approach is not recommended for patients with SHV. Optimal treatment for both SHV and OSA is positive airway pressure (PAP) which is highly effective if used; long-term compliance rates are 50 to 70%. PAP for OSA is applied at the same level throughout the respiratory cycle and works by pneumatically splinting open the UAW. For SHV treatment PAP cycles higher during inspiration; the differential pressure provides ventilatory support in addition to keeping the UAW patent.