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.

Vagal attenuation in panic disorder: an assessment of parasympathetic nervous system function and subjective reactivity to respiratory manipulations

Abstract: We examined the effects of hyperventilation and other manipulations of respiratory pace on parasympathetic nervous system function and subjective reactivity in 15 patients with panic disorder, 15 patients with social phobia, and 15 healthy control subjects. After a 30-minute rest period subjects completed a 2.5-minute trial of each of hypoventilation, normoventilation, and hyperventilation. Trials were separated by a 3 minute inter-trial interval. Incidence of panic attacks, symptom severity, vagal tone, heart rate, end-tidal carbon dioxide level, and respiratory frequency were measured throughout. Resting physiological measures did not differ between groups. Each respiratory manipulation resulted in the expected physiological changes (e.g., hyperventilation attenuated vagal tone), however, groups did not exhibit differential physiological reactivity to the manipulations. There were no panic attacks reported during either the hypoventilation or normoventilation phases; however, two social phobic subjects (13.3%) and two panic disorder patients (13.3%) reported panic attacks during hyperventilation. Although both groups of anxiety patients reported greater severity of hyperventilation-induced symptoms than did control subjects, symptom severity did not correlate significantly with vagal tone or heart rate. These results suggest that parasympathetic function is unlikely to be aberrant in PD patients and that diminished parasympathetic activity is not sufficient for the experience of panic attacks.

The influence of gender and upper airway resistance on the ventilatory response to arousal in obstructive sleep apnoea in humans.

Abstract: The termination of obstructive respiratory events is typically associated with arousal from sleep. The ventilatory response to arousal may be an important determinant of subsequent respiratory stability/instability and therefore may be involved in perpetuating obstructive respiratory events. In healthy subjects arousal is associated with brief hyperventilation followed by more prolonged hypoventilation on return to sleep. This study was designed to assess whether elevated sleeping upper airway resistance (RUA) alters the ventilatory response to arousal and subsequent breathing on return to sleep in patients with obstructive sleep apnoea (OSA). Inspired minute ventilation (VI), RUA and end-tidal CO2 pressure (PET,CO2) were measured in 22 patients (11 men, 11 women) with OSA (mean ±s.e.m., apnoea–hypopnoea index (AHI) 48.9 ± 5.9 events h−1) during non-rapid eye movement (NREM) sleep with low RUA (2.8 ± 0.3 cmH2O l−1 s; optimal continuous positive airway pressure (CPAP) = 11.3 ± 0.7 cmH2O) and with elevated RUA (17.6 ± 2.8 cmH2O l−1 s; sub-optimal CPAP = 8.4 ± 0.8 cmH2O). A single observer, unaware of respiratory data, identified spontaneous and tone-induced arousals of 3–15 s duration preceded and followed by stable NREM sleep. VI was compared between CPAP levels before and after spontaneous arousal in 16 subjects with tone-induced arousals in both conditions. During stable NREM sleep at sub-optimal CPAP, PET,CO2 was mildly elevated (43.5 ± 0.8 versus 42.5 ± 0.8 Torr). However, baseline VI (7.8 ± 0.3 versus 8.0 ± 0.3 l min−1) was unchanged between CPAP conditions. For the first three breaths following arousal, VI was higher for sub-optimal than optimal CPAP (first breath: 11.2 ± 0.9 versus 9.3 ± 0.6 l min−1). The magnitude of hypoventilation on return to sleep was not affected by the level of CPAP and both obstructive and central respiratory events were rare following arousal. Similar results occurred after tone-induced arousals which led to larger responses than spontaneous arousals. VI for the first breath following arousal under optimal CPAP was greater in men than women (11.0 ± 0.4 versus 7.6 ± 0.6 l min−1). These results demonstrate that the ventilatory response to arousal is influenced by pre-arousal airway resistance and gender. Whether this contributes to the perpetuation of respiratory events and the pathogenesis of OSA is unclear.

Hypoventilation during sleep in children who have lymphoid airway obstruction treated by nasopharyngeal tube and T and A.

Abstract: Three children with sleep apnea, alveolar hypoventilation, apparent mental retardation, and poor growth associated with chronically enlarged tonsils and adenoids were treated with the use of a nasopharyngeal tube followed by tonsillectomy and adenoidectomy. The effectiveness of this therapy was documented by polygraphic recording of sleep stages and respirations, and by correlation with serial arterial blood gases and pH. The nasopharyngeal tube was well tolerated, easy to use, and effective in diagnosis and treatment. We suggest that its use be further evaluated in patients with obstructive apnea.

Opioid-induced respiratory depression is associated with increased tidal volume variability

Abstract: SummaryBackground and objective: μ-agonistic opioids cause concentration-dependent hypoventilation and increased irregularity of breathing The aim was to quantify opioid-induced irregularity of breathing and to investigate its time-course during and after an opioid infusion, and its ability to predict the severity of respiratory depressionMethods: Twenty-three patients breathing spontaneously via a continuous positive airway pressure (CPAP) mask received an intravenous (iv) infusion of alfentanil (23 μg kg−1 min−1, 14 patients) or pirinitramide (piritramide) (179 μg kg−1 min−1, nine patients) until either a cumulative dose of 70 μg kg−1 for alfentanil or 500 μg kg−1 for pirinitramide had been achieved or the infusion had to be stopped for safety reasons Tidal volumes (VT) and minute ventilation were measured with an anaesthesia workstation For every 20 breaths, the quartile coefficient was calculated (Qeff20VT)Results: Both the decrease of minute volume and the increase of Qeff20VT during and after opioid infusion were highly significant (P < 0001, ANOVA) Patients in which the alfentanil infusion had to be terminated prematurely had lower minute volumes (P = 0002, t-test) and higher Qeff20VT (P = 0034, t-test) than those who received the complete dose Changes in the regularity of breathing measured as Qeff20VT parallel those of minute ventilation during and after opioid infusionConclusions: Opioids cause a more complicated disturbance of the control of respiration than a mere resetting to higher PCO2 Furthermore, Qeff20VT appears to predict the severity of opioid-induced respiratory depression

Syndrome of extreme obesity and hypoventilation: studies of etiology

Abstract: Excerpt The syndrome of extreme obesity, hypoventilation, polycythemia and heart failure has been recognized with increasing frequency since 1955.1-18The most characteristic cardiorespiratory dysfu...