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.

Limitations of split-night polysomnography for the diagnosis of nocturnal hypoventilation and titration of non-invasive positive pressure ventilation in amyotrophic lateral sclerosis.

Abstract: Split-night polysomnography is performed at our centre in all patients with ALS who require assessment for nocturnal hypoventilation and their response to non-invasive ventilation. The purpose of this study was to determine how successful this practice has been, reflected by whether a complete assessment was achieved by a single split-night polysomnogram. We undertook a systematic, retrospective review of all consecutive split-night polysomnograms in ALS patients between 2005 and 2012. A total of 47 cases were reviewed. Forty-three percent of patients had an incomplete test, resulting in a recommendation to repeat the polysomnogram. Poor sleep efficiency and absence of REM sleep in the diagnostic portion of the study were strongly associated with incomplete studies. Clinical variables that reflect severity of ALS (FVC, PaCO2, ALSFRS-R) and use of REM-suppressing antidepressants or sedative-hypnotics were not associated with incomplete split-night polysomnogram. In conclusion, a single, split-night polysomnogram is frequently inconclusive for the assessment of nocturnal hypoventilation and complete titration of non-invasive positive pressure ventilation in patients with ALS. Poor sleep efficiency and absence of REM sleep are the main limitations of split-night polysomnography in this patient population.

Chemoreflex failure and sleep-disordered breathing in familial dysautonomia: Implications for sudden death during sleep.

Abstract: Familial dysautonomia (Riley-Day syndrome, hereditary sensory and autonomic neuropathy type III) is a rare autosomal recessive disease characterized by impaired development of primary sensory and autonomic neurons resulting in a severe neurological phenotype, which includes arterial baroreflex and chemoreflex failure with high frequency of sleep-disordered breathing and sudden death during sleep. Although a rare disease, familial dysautonomia represents a unique template to study the interactions between sleep-disordered breathing and abnormal chemo- and baroreflex function. In patients with familial dysautonomia, ventilatory responses to hypercapnia are reduced, and to hypoxia are almost absent. In response to hypoxia, these patients develop paradoxical hypoventilation, hypotension, bradycardia, and potentially, death. Impaired ventilatory control due to chemoreflex failure acquires special relevance during sleep when conscious control of respiration withdraws. Overall, almost all adult (85%) and pediatric (95%) patients have some degree of sleep-disordered breathing. Obstructive apnea events are more frequent in adults, whereas central apnea events are more severe and frequent in children. The annual incidence rate of sudden death during sleep in patients with familial dysautonomia is 3.4 per 1000 person-year, compared to 0.5-1 per 1000 person-year of sudden unexpected death in epilepsy. This review summarizes recent developments in the understanding of sleep-disordered breathing in patients with familial dysautonomia, the risk factors for sudden death during sleep, and the specific interventions that could prevent it.

Relation of ventricular fibrillation threshold to heart rate during normal ventilation and hypoventilation in female Wistar rats: a chronophysiological study.

Abstract: The aim of our study was to verify the relationship between heart rate (HR) and ventricular fibrillation threshold (VFT) during different types of ventilation in female Wistar rats from the circadian point of view The experiments were performed under pentobarbital anesthesia (40 mg/kg ip, adaptation to a light-dark cycle 12:12 h, open chest experiments) and the obtained results were averaged independently of the seasons The VFT measurements were performed during normal ventilation (17 animals) and hypoventilation (10 animals) The HR was recorded immediately before the rise of ventricular arrhythmias Results are expressed as arithmetic means -/+ SD and differences are considered significant when p<005 The basic periodic characteristics were calculated using single and population mean cosinor tests The results from our experiments have demonstrate that 1) the VFT and HR respond identically to hypoventilation by a decrease in the light and also in the dark phases, and 2) hypoventilation changes the 24-h course of the VFT without a change in the 24-h rhythm of the HR It is concluded that the HR and VFT behave as two independent functional systems without apparent significant circadian dependence during both types of ventilation

[Central sleep apnea (Ondine's curse syndrome) in medullary infarction].

Abstract: Ondine's curse syndrome primarily refers to cases with congenital central alveolar hypoventilation, but the term can also be used for acquired cases and implies central sleep apnea that occurs as a manifestation or complication of focal lesion in the area of the dorsolateral segment of medulla oblongata. It occurs rarely, but can lead to fatal outcome. Based on our own case report, the aim of this article is to review its clinical symptoms, and appropriate diagnostic and therapeutic procedures. We present a patient who had symptoms of vascular lesion of the dorsolateral segment of the medulla, which was verified by magnetic resonance imaging. On day 12 of his hospital stay, in the early morning, rapid development of coma was observed, which was an expression of serious respiratory failure with dominant hypercapnia. In the beginning, urgent intubation and mechanical ventilation were necessary, while in the later course of the disease breathing was assisted by noninvasive methods of Bilevel Positive Airway Pressure (BiPAP) and Continuous Positive Airway Pressure (CPAP). Throughout the night, polygraph recording confirmed the diagnosis of the central sleep apnea syndrome. The course of the disease was favorable, with a very slow but constant improvement of respiratory function. According to literature data, the disease course is not always favorable. There are published cases where it was concluded that ventilatory support was no longer needed but after a long period of normal breathing hypoventilation and death occurred suddenly during sleep. The treatment of central hypoventilation consists of ventilatory support, but there were also attempts of medicamentous treatment with the common aim of raising alertness and reactibility of the automatic breathing center. It is important to emphasize that patients with the risk of central sleep apnea should not be supplied with oxygen without arterial blood gas monitoring because of the possibility of delaying the right diagnosis. The use of oxygen in patients who already have hypercapnia due to hypoventilation could further intensify hyporeactivity of the breathing center and lead to respiratory arrest.

Severe Hypoxemia Prevents Spontaneous and Naloxone-induced Breathing Recovery after Fentanyl Overdose in Awake and Sedated Rats

Abstract: Background As severe acute hypoxemia produces a rapid inhibition of the respiratory neuronal activity through a nonopioid mechanism, we have investigated in adult rats the effects of hypoxemia after fentanyl overdose-induced apnea on (1) autoresuscitation and (2) the antidotal effects of naloxone. Methods In nonsedated rats, the breath-by-breath ventilatory and pulmonary gas exchange response to fentanyl overdose (300 µg · kg · min iv in 1 min) was determined in an open flow plethysmograph. The effects of inhaling air (nine rats) or a hypoxic mixture (fractional inspired oxygen tension between 7.3 and 11.3%, eight rats) on the ability to recover a spontaneous breathing rhythm and on the effects of naloxone (2 mg · kg) were investigated. In addition, arterial blood gases, arterial blood pressure, ventilation, and pulmonary gas exchange were determined in spontaneously breathing tracheostomized urethane-anesthetized rats in response to (1) fentanyl-induced hypoventilation (7 rats), (2) fentanyl-induced apnea (10 rats) in air and hyperoxia, and (3) isolated anoxic exposure (4 rats). Data are expressed as median and range. Results In air-breathing nonsedated rats, fentanyl produced an apnea within 14 s (12 to 29 s). A spontaneous rhythmic activity always resumed after 85.4 s (33 to 141 s) consisting of a persistent low tidal volume and slow frequency rhythmic activity that rescued all animals. Naloxone, 10 min later, immediately restored the baseline level of ventilation. At fractional inspired oxygen tension less than 10%, fentanyl-induced apnea was irreversible despite a transient gasping pattern; the administration of naloxone had no effects. In sedated rats, when PaO2 reached 16 mmHg during fentanyl-induced apnea, no spontaneous recovery of breathing occurred and naloxone had no rescuing effect, despite circulation being maintained. Conclusions Hypoxia-induced ventilatory depression during fentanyl induced apnea (1) opposes the spontaneous emergence of a respiratory rhythm, which would have rescued the animals otherwise, and (2) prevents the effects of high dose naloxone.