Topic
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.
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TL;DR: Attempts to alleviate etorphine-induced hypoxia should focus not only on reversing the opioid-induced respiratory depression, but also on improving gas exchange by preventing etorphin-induced pulmonary hypertension.
Abstract: Background: Etorphine, a potent opioid agonist, causes pulmonary hypertension and respiratory depression. Whether etorphine-induced pulmonary hypertension negatively influences pulmonary gas exchange and exacerbates the effects of ventilator depression and the resultant hypoxemia is unknown. To determine if these effects occurred we instrumented twelve goats with peripheral and pulmonary arterial catheters to measure systemic and pulmonary pressures before and after etorphine administration. Concurrent cardiopulmonary and arterial blood gas variables were also measured. Results: Etorphine induced hypoventilation (55% reduction to 7.6 ± 2.7 L.min �1 ,F (11,44) = 15.2 P 40 mmHg, F(11,44) = 5.6 P< 0.0001) and pulmonary hypertension (mean 23 ± 6 mmHg, F(11,44) = 8.2 P < 0.0001). Within 6 min of etorphine administration hypoxia was twice (F(11,22) =3 .0P < 0.05) as poor than that expected from etorphine-induced hypoventilation alone. This disparity appeared to result from a decrease in the movement of oxygen (gas exchange) across the alveoli membrane, as revealed by an increase in the P(A-a)O2 gradient (F(11,44) =7 .9P < 0.0001). The P(A-a)O2 gradient was not correlated with global changes in the ventilation perfusion ratio (P = 0.28) but was correlated positively with the mean pulmonary artery pressure (P = 0.017, r 2 = 0.97), indicating that pulmonary pressure played a significant role in altering pulmonary gas exchange. Conclusion: Attempts to alleviate etorphine-induced hypoxia therefore should focus not only on reversing the opioid-induced respiratory depression, but also on improving gas exchange by preventing etorphine-induced pulmonary hypertension.
38 citations
Journal Article•
TL;DR: To stimulate pulmonary and thoracic growth, intermittent ventilatory assistance by pressure preset ventilator should be performed as soon as possible and pursued up to 8 years of age, at least, more if necessity, to prevent respiratory insufficiency.
Abstract: In kyphoscoliosis restrictive ventilatory defect occurs. In idiopathic scoliosis vital capacity failure is significantly correlated with Cobb angle, vertebral rotation, and thoracic lordosis. Maximum voluntary ventilation is the most affected measurement. Forced expiratory volume in 1 second is reduced. Residual volume remains longtime normal. Hypoxemia due to decrease of diffusing capacity occurs, with initially reflex hyperventilation hypocapnia, and secondary hypercapnia. Pulmonary hypertension and cor pulmonale is related to hypoventilation and hypoxia. The lung situated on the concave side of the scoliosis curve shows a more functional derangement. Ventilatory pattern consists of low tidal volume and high respiratory rate with increase of ventilatory work. Scoliosis that appears in the earlier stage of the life has the worst respiratory prognosis (before 5 years of age) with impairement of lung and thoracic growth. To stimulate pulmonary and thoracic growth, intermittent ventilatory assistance by pressure preset ventilator should be performed as soon as possible and pursued up to 8 years of age, at least, more if necessity. In over 60 degrees angle idiopathic scoliosis, respiratory failure appears after 40 to 50 years of age. Non invasive ventilatory assistance with preset pressure ventilator by oral way in moderate cases and nocturnal nasal ventilation by volume ventilator or inspiratory assistance ventilator, in the most severe cases are efficient. In very severe and acute respiratory insufficiency (scoliosis over 90 degrees) ventilation by intubation then tractheostomy may be required. Earlier orthopedic management and surgical procedure to correct and stabilize spinal deformities is the best to prevent respiratory insufficiency. For scoliosis below 60 degrees, post operative pulmonary complications are very low, with no requirement of post operative ventilatory support. In very severe respiratory insufficiency treatment of respiratory failure precedes, and follows, orthotic treatment and surgical procedures; it shouldle pursued afterwards.
38 citations
TL;DR: Investigation of the effects of hyper- and hypoventilation on gastric and sublingual tissue PCO(2) before, during, and after reversal of hemorrhagic shock found statistically similar decreases and increases in Pg(CO)2 and Psl(CO(2).
Abstract: We investigated the effects of hyper- and hypoventilation on gastric ( Pg CO 2 ) and sublingual (P sl CO 2 ) tissue P CO 2 before, during, and after reversal of hemorrhagic shock. Pg CO 2 was measu...
38 citations
TL;DR: Though the etiology of rapid onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation is still to be determined, recent studies have begun to carefully delineate the phenotype, suggesting that it too may provide fertile ground for research that both advances the authors' knowledge and improves patient care.
Abstract: Respiratory and autonomic disorders of infancy, childhood, and adulthood are a group of disorders that have varying presentation, combined with a range of severity of respiratory control and autonomic nervous system dysfunction. Within this group, congenital central hypoventilation syndrome and rapid onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation, exhibit the greatest respiratory control deficits, requiring supported ventilation as a mainstay of care. The discovery of the key role of the paired-like homeobox 2B gene in autonomic nervous system development, along with the identification of paired-like homeobox 2B gene mutations causing congenital central hypoventilation syndrome, has led to a fruitful dialog between basic scientists and physician-scientists, producing an explosion of knowledge regarding genotype-phenotype correlations in this disorder, as well as important animal models of chemosensory regulation deficit. Though the etiology of rapid onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation is still to be determined, recent studies have begun to carefully delineate the phenotype, suggesting that it too may provide fertile ground for research that both advances our knowledge and improves patient care.
38 citations
TL;DR: Children with ROHHAD may initially present with OSA and only develop NH later as well as dysregulation of breathing during wakefulness, and the recognition of the spectrum of respiratory abnormalities at presentation and over time may be important in raising the index of suspicion of RohHAD.
Abstract: Rapid-onset obesity with hypothalamic dysfunction, hypoventilation and autonomic dysregulation (ROHHAD) is a rare disease with a high mortality rate. Although nocturnal hypoventilation (NH) is central to ROHHAD, the evolution of sleep disordered breathing (SDB) is not well studied. The aim of the study was to assess early manifestations of SDB and their evolution in ROHHAD syndrome. Retrospective study of children with ROHHAD at two Canadian centers. All children with suspected ROHHAD at presentation underwent polysomnography (PSG) to screen for nocturnal hypoventilation. PSG findings at baseline and follow-up were collected. Interventions and diagnostic test results were recorded. Six children were included. The median age of rapid onset obesity and nocturnal hypoventilation (NH) was 3.5 and 7.2 years respectively. On initial screening for ROHHAD 4/6 (66.7 %) children had obstructive sleep apnea (OSA), 1/6 (16.7 %) had NH and 1/6 (16.7 %) had both OSA and NH. Follow up PSGs were performed in 5/6 children as one child died following a cardiorespiratory arrest. All children at follow up had NH and required non-invasive positive pressure ventilation. Additionally, 3/6 (50 %) children demonstrated irregular breathing patterns during wakefulness. Children with ROHHAD may initially present with OSA and only develop NH later as well as dysregulation of breathing during wakefulness. The recognition of the spectrum of respiratory abnormalities at presentation and over time may be important in raising the index of suspicion of ROHHAD. Early recognition and targeted therapeutic interventions may limit morbidity and mortality associated with ROHHAD.
38 citations