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: The hyperventilation in response to hypercapnia increases as maturation proceeds and the maturation of the peripheral chemoreceptors contribute to this effect, as during hypoxia.
Abstract: In conscious newborns, the ventilatory response to hypoxia is characterized by precocious hyperventilation followed by tardive hypoventilation, the latter disappearing with age The hypoventilation could be mainly related to a weak peripheral drive and to the persistence of the diaphragmatic activity during expiration Also, a decrease in metabolic rate and body temperature interferes with the response The hyperventilation in response to hypercapnia increases as maturation proceeds and the maturation of the peripheral chemoreceptors contribute to this effect, as during hypoxia The responses to both stimuli depend on many factors such as sleep state, anesthesia or ambient temperature
22 citations
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TL;DR: A mixed breed dog presented with generalized weakness, hypoventilation and hypoxemia and had persistent cervical ventroflexion for a total of 4 weeks.
Abstract: Objective: To discuss a new clinical presentation of organophosphate toxicity called the intermediate syndrome in a dog
Case summary: A mixed breed dog presented with generalized weakness, hypoventilation and hypoxemia The weakness was most marked in the thoracic limbs, cervical and respiratory muscles The history revealed a likely exposure to an organophosphate compound The other dog in the household demonstrated mild clinical signs of organophosphate toxicity A blood cholinesterase level was markedly reduced Therapy included placement of a tracheostomy tube and mechanical ventilation The dog gradually improved over the following 8 days but had persistent cervical ventroflexion for a total of 4 weeks
New or unique information provided: Organophosphate toxicity can present as a paralysis following the acute cholinergic crisis The muscular weakness predominantly affects the thoracic limb and neck muscles but cranial nerve deficits can also occur Dogs can die from the associated respiratory depression Oxime therapy is indicated in the treatment of this syndrome
21 citations
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TL;DR: A 15-year-old obese boy with an acute febrile encephalopathy had hypoventilation, autonomic dysfunction, visual hallucinations, hyperekplexia, and disordered body temperature, and saltwater regulation.
21 citations
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TL;DR: The data suggest that both delta- and mu-agonists induce alveolar hypoventilation despite a decrease in VO2, and that endorphins do not modulate ventilation and metabolic rate tonically, but it is speculated that they may do so in response to stressful stimulation.
Abstract: To study the effect of endorphins on metabolic rate and on the relationship between O2 consumption (VO2) and ventilation, we administered enkephalin analogues (relatively selective delta-receptor agonists) and a morphiceptin analogue (a highly selective mu-receptor agonist) intracisternally in nine unanesthetized chronically instrumented adult dogs. Both delta- and mu-agonists decreased VO2 by 40-60%. delta-Agonists induced a dose-dependent decrease in mean instantaneous minute ventilation (VT/TT) associated with periodic breathing. The decrease in VT/TT started and resolved prior to the decrease and returned to baseline of VO2, respectively. In contrast, the mu-agonists induced an increase in VT/TT associated with rapid shallow breathing. Arterial PCO2 increased and arterial PO2 decreased after both delta- and mu-agonists. Low doses of intracisternal naloxone (0.002-2.0 micrograms/kg) reversed the opioid effect on VT/TT but not on VO2; higher doses of naloxone (5-25 micrograms/kg) reversed both. Naloxone administered alone had no effect on VT/TT or VO2. These data suggest that 1) both delta- and mu-agonists induce alveolar hypoventilation despite a decrease in VO2, 2) this hypoventilation results from a decrease in VT/TT after delta-agonists but an increase in dead space ventilation after mu-agonists, and 3) endorphins do not modulate ventilation and metabolic rate tonically, but we speculate that they may do so in response to stressful stimulation.
21 citations