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.

Asthma: pathophysiology of the bronchial obstruction

Abstract: From a pathophysiologic perspective, the changes that occur in asthma are multiple, diverse, and complex. Assessment of the mechanical properties of the ventilatory apparatus provides several different types of information, depending on the gravity of the bronchial obstruction. During asthma, or induced bronchial obstruction, the function of the muscles is altered, causing changes in respiratory timing. Expiratory duration decreases more than inspiratory duration, and the functional residual capacity (FRC) increases, due to mechanical changes within the airways that lead to air trapping. The related hypoventilation is responsible for hypoxemia and hypercapnia, but it does not severely affect the diffusion capacity of the alveolocapillary membrane. We describe the pathophysiology of the bronchial obstruction in asthmatic patients, underlining the critical function of the respiratory muscles. Moreover, we clarify the relations between the ventilatory changes and gas-exchange alteration.

Pathophysiology of the obesity hypoventilation syndrome

Abstract: The obesity hypoventilation syndrome (OHS) is defined by extreme overweight (BMI 30 kg/m2), daytime hypoventilation (PaCO2 > 45 mm Hg, the absence of other known causes of hypoventilation) and sleep-related breathing disorders. Obesity impairs breathing due to a restrictive ventilatory disorder, reduction of the capacity of respiratory muscles and diminishment of the ventilatory response. The restriction cannot serve as the only explanation of OHS because body weight or compliance on the one hand and hypoventilation on the other hand only correlate weakly. Obesity increases the work of breathing by greater body mass with its increased oxygen demand, impaired diaphragmatic mobility, upper airway obstruction, and oxygen desaturation which result in an inadequacy of oxygen demand and supply. The adjustment of the chemoreceptors can avoid the overload on the capacity of the respiratory muscles, at least in a number of patients or in the course of the disease. This disproportion results in hypercapnia. Furthermore, the level of leptin is an important factor in the pathophysiology of OHS. The blood level of leptin correlates with the body fat mass in humans. However, there seems to be a relative leptin deficiency in the brain in overweight humans. Therefore, in contrast to animals, leptin cannot sufficiently increase ventilation in man to avoid hypercapnia.

Congenital central hypoventilation syndrome and the PHOX2B gene mutation.

Abstract: Congenital central hypoventilation syndrome (CCHS) is a rare syndrome of dysfunction of the autonomic nervous system characterized by a decreased response to hypercarbia. It is a disorder in which affected individuals fail to breathe during sleep despite progressive hypercapnia and hypoxia. Infants simply fall asleep and quit breathing. They are found by their parents or caregivers blue and lifeless. CCHS is an autosomal dominant disease. It has been linked with tumors of neural crest origin, segmental aganglionosis of the colon, and diffuse autonomic dysregulation but can occur alone. Discovery of the genetic link between the paired-like homeobox 2B (PHOX2B) genetic mutations and CCHS represents a breakthrough in the diagnosis of CCHS, association of mutated alleles with disease severity, and clues to the pathophysiology responsible for the disorder. Early genetic screening and intervention can provide the families of these infants with hope for achieving a normal life.

Congenital hypoventilation syndromes

Abstract: Although rare, congenital hypoventilation syndromes profoundly impact affected patients and families. In some diseases, such as congenital central hypoventilation syndrome (CCHS), hypoventilation is a key presenting feature. Ventilatory abnormalities may not be immediately evident in other disease states. The clinical aspects of several pediatric hypoventilation syndromes, including CCHS, Chiari type II malformation, Prader-Willi syndrome, familial dysautonomia, and rapid onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation are presented.