Hypoventilation

About: Hypoventilation is a research topic. Over the lifetime, 1772 publications have been published within this topic receiving 40799 citations. The topic is also known as: respiratory depression.

Ondine's Curse - Genetic and Iatrogenic Central Hypoventilation as Diagnostic Options in Forensic Medicine.

Abstract: In the Nordic mythology a man lost his ability to breathe without remembering it after he was cursed by water nymph - referred to as ‘Ondine’s curse’ – and then he died as soon as he fell asleep. Family medicine specialists are familiar with many sleeping disorders that their patients commonly call by the term Ondine’s Curse. In medical sciences this term is historically related to the group of conditions that have as the common denominator seemingly spontaneous onset of life-threatening hypoventilation. The physiology and genetics specialists focus mainly on congenital central hypoventilation syndrome (CCHS), which was proven to be linked to several genetic mutations. Anesthesiologists tend to be more interested in similarly manifesting iatrogenic condition. Typically, patients that were previously subjected to general anesthesia, after temporarily waking up and regaining the spontaneous respiratory drive, later fall back into unconsciousness and develop hypoventilation. Anesthesiologists also call it Ondine’s curse because of the sudden and unexpected sleep onset. The iatrogenic Ondine’s curse is proven to be precipitated by delayed anesthetics release from patients’ fat tissue – where it was deposited at the time general anesthesia was administered – back into bloodstream. Forensic medicine has to consider the latter form of Ondine’s curse called scenario more often, as they investigate sudden deaths related to surgery and general anesthesia in the post-operational care period. These cases may also fall into the category of medical malpractice-related deaths.

Hypothyroidism and Alveolar Hypoventilation

Abstract: THE PATIENT with a hypoventilation syndrome1generally complains of easy fatigability, hypersomnolence, and morning headaches and exhibits irritability and mental deterioration. Dyspnea is rarely prominent unless lung disease is present. On examination, tremor, twitching, cyanosis, and irregular respiration may be observed. The irregularity in respiration is particularly apparent during sleep. There may be evidence of right ventricular hypertrophy which can be confirmed by roentgenograms of the chest and/or the electrocardiogram. Polycythemia without leukocytosis or thrombocytosis and an elevated serum bicarbonate are common. The essential finding is an elevated arterial carbon dioxide tension (paCO2). Although hypoxemia is usually present, normal arterial oxygen tensions may be recorded if the patient has hyperventilated immediately prior to the study. With such an increase in ventilation, hypoxemia is reversed quickly, but the carbon dioxide retention is corrected more slowly. The etiology of this syndrome is varied (Fig 1). Most frequently it is the

Successful treatment of respiratory dysfunction in cystinosis by nocturnal non-invasive positive pressure ventilation.

Abstract: Cystinosis is a rare metabolic disorder characterized by lysosomal cystine accumulation leading to multi-organ damage, with kidneys being clinically first affected. Longer survival of cystinosis patients due to successful renal replacement therapy, revealed previously unknown extra-renal symptoms of cystinosis, generally appearing after the first decade. Respiratory insufficiency caused by overall respiratory muscle myopathy is a severely invalidating and sometimes a life-threatening complication of cystinosis. We report a successful treatment of hypoventilation, due to diaphragm myopathy in a cystinosis patient, by nocturnal non-invasive positive pressure ventilation (NIPPV). After initiation of NIPPV the clinical condition of the patient improved and blood-gasses normalized, indicating that this treatment modality should be considered in cystinosis patients with severe respiratory insufficiency.

Sleep hypoventilation syndrome and respiratory failure due to multifocal motor neuropathy with conduction block.

Abstract: Sleep hypoventilation syndrome and respiratory failure have been reported in association with a diverse spectrum of neuromuscular disorders. We report a patient with multifocal motor neuropathy with conduction block who presented with sleep hypoventilation, presumably due to bilateral phrenic neuropathy and was initially diagnosed to have obstructive sleep apnea syndrome. Once the correct diagnosis was made the patient was treated successfully with a combination of regular immunoglobulin and bilevel nocturnal ventilation. Delay in the administration of intravenous immunoglobulin resulted in respiratory failure. Muscle Nerve, 2011

Acute Respiratory Failure in Obesity-Hypoventilation Syndrome Managed in the ICU.

Abstract: BACKGROUND: Obesity-hypoventilation syndrome (OHS) is defined as the combination of obesity (body mass index ≥ 30 kg/m2) and daytime arterial hypercapnia (PaCO2 > 45 mm Hg) in the absence of other causes of hypoventilation, and can lead to acute hypercapnic respiratory failure in the ICU. Our objective was to describe the ventilatory management and outcomes of subjects with OHS who were admitted to the ICU for acute hypercapnic respiratory failure. METHODS: We retrospectively built a cohort of subjects with OHS who were admitted for acute hypercapnic respiratory failure in 4 ICUs of the university teaching hospital in Lyon, France, between 2013 and 2017. The main end point was the rate of success of noninvasive ventilation (NIV). Secondary end points were survival from OHS diagnosis to the last follow-up and risk factors for ICU admission and long-term survival. RESULTS: One hundred fifteen subjects with OHS were included. Thirty-seven subjects (32.1%) were admitted to the ICU for acute hypercapnic respiratory failure. Congestive heart failure was the leading cause of acute hypercapnic respiratory failure (54%). At ICU admission, pH before NIV use was median (range) 7.26 (7.22–7.31) and PaCO2 was 70 (61–76) mm Hg. NIV was used as first-line ventilatory support in 36 subjects (97.2%) and was successful in 33 subjects (91.7%). ICU mortality was low (2.7%). The subjects admitted to the ICU were significantly older and had a lower FEV1 and vital capacity at the time of an OHS diagnosis. The difference in the restricted mean survival time was 663 d in favor of subjects not admitted to the ICU. Multivariate analysis showed that lower vital capacity at an OHS diagnosis was significantly associated with a higher risk of ICU admission. No factor was independently associated with long-term overall mortality in multivariate analysis. CONCLUSIONS: Acute hypercapnic respiratory failure in subjects with OHS was generally responsive to NIV and was frequently associated with congestive heart failure.