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1
Schagatay, Erika, Johan P. A. Andersson, Magnus Hallén, and Birger Pålsson. "Selected Contribution: Role of spleen emptying in prolonging apneas in humans." Journal of Applied Physiology 90, no. 4 (April 1, 2001): 1623–29. http://dx.doi.org/10.1152/jappl.2001.90.4.1623.
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This study addressed the interaction between short-term adaptation to apneas with face immersion and erythrocyte release from the spleen. Twenty healthy volunteers, including ten splenectomized subjects, participated. After prone rest, they performed five maximal-duration apneas with face immersion in 10°C water, with 2-min intervals. Cardiorespiratory parameters and venous blood samples were collected. In subjects with spleens, hematocrit and hemoglobin concentration increased by 6.4% and 3.3%, respectively, over the serial apneas and returned to baseline 10 min after the series. A delay of the physiological breaking point of apnea, by 30.5% (17 s), was seen only in this group. These parameters did not change in the splenectomized group. Plasma protein concentration, preapneic alveolar Pco 2, inspired lung volume, and diving bradycardia remained unchanged throughout the series in both groups. Serial apneas thus triggered the hematological changes that have been previously observed after long apneic diving shifts; they were rapidly reversed and did not occur in splenectomized subjects. This suggests that splenic contraction occurs in humans as a part of the diving response and may prolong repeated apneas.
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Dhakal, Y., B. Bhattarai, S. Khatiwada, and A. Subedi. "Effect of Positive Airway Pressure During Preoxygenation on Safe Apnea Period: a comparison of the supine and 25° head up position." Kathmandu University Medical Journal 18, no. 2 (December 6, 2020): 62–67. http://dx.doi.org/10.3126/kumj.v18i2.33258.
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Background Preoxygenation is performed before induction of anaesthesia which increases oxygen reserve and provides delayed onset of hypoxia during period of apnea. Several techniques such as positive airway pressure and head-up tilt during preoxygenation have shown to prolong safe apnea period compared to conventional technique. However, uniform recommendations have not yet been made.
Objective To find out the effect of combination of 5 cmH2O continuous positive airway pressure (CPAP) and 25° head up position during preoxygenation on safe apnea period.
Method In this comparative study 60 non-obese adult patients were divided into three equal groups; Group C receiving preoxygenation in conventional technique, Group S receiving preoxygenation with 5 cmH2O continuous positive airway pressure in supine position and Group H receiving preoxygenation in 25° head-up position with 5 cmH2O continuous positive airway pressure . After 3 min of preoxygenation, intubation was performed after induction of anaesthesia with propofol, fentanyl and succinylcholine. After confirming the tracheal intubation by direct visualization, all patients were administered vecuronium to maintain neuromuscular blockade. Post-intubation, patients in all groups were left in same position with the tracheal tube exposed to atmosphere and without being ventilated till the SpO2 dropped to 92%. The primary outcome compared between the groups was the safe apnea period (time from loss of consciousness to fall of SpO2 to 92%).
Result The duration of safe apnea period was longer (p < 0.05) in Group H patients (405.9 ± 106.69 s) as compared to the Group C (296.9 ± 99.01s) and Group S (319.65 ± 71.54s). Although the duration of safe apnea period was longer in the Group S as compared to Group C the difference was not statistically significant.
Conclusion Preoxygenation in 25° head-up position with 5 cmH2O continuous positive airway pressure significantly prolongs safe apnea period in non-obese adults compared to supine position, with or without 5 cmH2O continuous positive airway pressure.
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Leevers, A. M., P. M. Simon, and J. A. Dempsey. "Apnea after normocapnic mechanical ventilation during NREM sleep." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2079–85. http://dx.doi.org/10.1152/jappl.1994.77.5.2079.
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We determined whether normocapnic mechanical ventilation at high tidal volume (VT) and breathing frequency (f) during non-rapid-eye-movement (NREM) sleep would cause apnea. Seven normal sleeping subjects were placed on assist-control mechanical ventilation (i.e., subject initiates inspiration) and VT was gradually increased to 2.1 times eupneic VT (1.17 +/- 0.04 liters). This high VT was maintained for 5 min, the ventilator mode was switched to controlled mechanical ventilation, and f was increased gradually from 9.5 +/- 1.0 (during assist-control mechanical ventilation) to 14.0 +/- 0.7 breaths/min. Normocapnia (end-tidal PCO2 = 44 +/- 1.2 Torr) was maintained throughout the trials. Inspiratory effort was completely inhibited during the period of sustained high VT and f, and apnea occurred immediately after cessation of the passive mechanical ventilation. The duration of the apnea preceding the first inspiratory effort was 20.3 +/- 2.3 s or 7.1 times the eupneic expiratory duration and 5 times the expiratory duration chosen by the subject during assist-control mechanical ventilation. We conclude that inhibition of inspiratory motor output occurs during and after normocapnic mechanical ventilation at high VT and f during NREM sleep. These neuromechanical inhibitory effects may serve to initiate and prolong apnea.
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Porcaro, A., M. Romano, S. Maluta, M. Palazzi, F. Pioli, S. Dall'Oglio, A. D'Amico, L. Etta, C. Cavedon, and A. Rizzotti. "May Oxygen Hyperventilation Prolong Apnea in Patients Undergoing Radiation in Order to Reduce the Respiratory Movements?" International Journal of Radiation Oncology*Biology*Physics 78, no. 3 (November 2010): S825. http://dx.doi.org/10.1016/j.ijrobp.2010.07.1910.
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Xia, Luxi, Tracey Damon, Mary M. Niblock, Donald Bartlett, and J. C. Leiter. "Unilateral microdialysis of gabazine in the dorsal medulla reverses thermal prolongation of the laryngeal chemoreflex in decerebrate piglets." Journal of Applied Physiology 103, no. 5 (November 2007): 1864–72. http://dx.doi.org/10.1152/japplphysiol.00524.2007.
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The laryngeal chemoreflex (LCR) is elicited by water in the larynx and leads to apnea and respiratory disruption in immature animals. The LCR is exaggerated by the elevation of brain temperature within or near the nucleus of the solitary tract (NTS) in decerebrate piglets. Thermal prolongation of reflex apnea elicited by superior laryngeal nerve stimulation is reduced by systemic administration of GABAA receptor antagonists. Therefore, we tested the hypothesis that microdialysis within or near the NTS of gabazine, a GABAA receptor antagonist, would reverse thermal prolongation of the LCR. We examined this hypothesis in 21 decerebrate piglets (age 3–13 days). We elicited the LCR by injecting 0.1 ml of water into the larynx before and after each piglet's body temperature was elevated by ∼2.5°C and before and after 2–5 mM gabazine was dialyzed unilaterally and focally in the medulla. Elevated body temperature failed to prolong the LCR in one piglet, which was excluded from analysis. Elevated body temperature prolonged the LCR in all the remaining animals, and dialysis of gabazine into the region near the NTS ( n = 10) reversed the thermal prolongation of the LCR even though body temperature remained elevated. Dialysis of gabazine in other medullary sites ( n = 10) did not reverse thermal prolongation of the LCR. Gabazine had no consistent effect on baseline respiratory activity during hyperthermia. These findings are consistent with the hypothesis that hyperthermia activates GABAergic mechanisms in or near the NTS that are necessary for the thermal prolongation of the LCR.
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Arbour, Richard. "Cardiogenic Oscillation and Ventilator Autotriggering in Brain-Dead Patients: A Case Series." American Journal of Critical Care 18, no. 5 (September 1, 2009): 496–88. http://dx.doi.org/10.4037/ajcc2009690.
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Brain death is manifested by a flaccid, areflexic patient on assessment of brain function with fixed and dilated pupils at midpoint, loss of consciousness, no response to stimulation, loss of brainstem reflexes, and apnea. A lesion or clinical state responsible for the loss of consciousness must be found. An integral part of clinical evaluation of brain death is apnea testing, which indicates complete loss of brainstem function and respiratory drive. Ventilator triggering or overbreathing the ventilator’s set rate may be considered consistent with intrinsic respiratory drive consequent to residual brainstem function. Ventilator autotriggering, however, may potentially occur in a brain-dead patient as a result of interaction between the hyperdynamic cardiovascular system and compliant lung tissue altering airway pressure and flow patterns. Also, chest wall and pre-cordial movements may mimic intrinsic respiratory drive. Ventilator autotriggering may delay determination of brain death, prolong the intensive care unit experience for patients and their families, increase costs, risk loss of donor organs, and confuse staff and family members. A detailed literature review and 3 cases of cardiogenic ventilator autotriggering are presented as examples of this phenomenon and highlight the value of close multidisciplinary clinical evaluation and examination of ventilator pressure and flow waveforms.
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Andersson, Johan P. A., Mats H. Linér, Anne Fredsted, and Erika K. A. Schagatay. "Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans." Journal of Applied Physiology 96, no. 3 (March 2004): 1005–10. http://dx.doi.org/10.1152/japplphysiol.01057.2002.
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The effect of the diving response on alveolar gas exchange was investigated in 15 subjects. During steady-state exercise (80 W) on a cycle ergometer, the subjects performed 40-s apneas in air and 40-s apneas with face immersion in cold (10°C) water. Heart rate decreased and blood pressure increased during apneas, and the responses were augmented by face immersion. Oxygen uptake from the lungs decreased during apnea in air (-22% compared with eupneic control) and was further reduced during apnea with face immersion (-25% compared with eupneic control). The plasma lactate concentration increased from control (11%) after apnea in air and even more after apnea with face immersion (20%), suggesting an increased anaerobic metabolism during apneas. The lung oxygen store was depleted more slowly during apnea with face immersion because of the augmented diving response, probably including a decrease in cardiac output. Venous oxygen stores were probably reduced by the cardiovascular responses. The turnover times of these gas stores would have been prolonged, reducing their effect on the oxygen uptake in the lungs. Thus the human diving response has an oxygen-conserving effect.
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Roshan Lal, Tamanna, Gurpreet K. Seehra, Alta M. Steward, Chelsie N. Poffenberger, Emory Ryan, Nahid Tayebi, Grisel Lopez, and Ellen Sidransky. "The natural history of type 2 Gaucher disease in the 21st century." Neurology 95, no. 15 (August 6, 2020): e2119-e2130. http://dx.doi.org/10.1212/wnl.0000000000010605.
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ObjectiveTo gather natural history data to better understand the changing course of type 2 Gaucher disease (GD2) in order to guide future interventional protocols.MethodsA structured interview was conducted with parents of living or deceased patients with GD2. Retrospective information obtained included disease presentation, progression, medical and surgical history, medications, family history, management, complications, and cause of death, as well as the impact of disease on families.ResultsData from 23 patients were analyzed (20 deceased and 3 living), showing a mean age at death of 19.2 months, ranging from 3 to 55 months. Fourteen patients were treated with enzyme replacement therapy, 2 were treated with substrate reduction therapy, and 3 underwent bone marrow transplantation. Five patients received ambroxol and one was on N-acetylcysteine, both considered experimental treatments. Fifteen patients had gastrostomy tubes placed; 10 underwent tracheostomies. Neurologic disease manifestations included choking episodes, myoclonic jerks, autonomic dysfunction, apnea, seizures, and diminished blinking, all of which worsened as disease progressed.ConclusionsCurrent available therapies appear to prolong life but do not alter neurologic manifestations. Despite aggressive therapeutic interventions, GD2 remains a progressive disorder with a devastating prognosis that may benefit from new treatment approaches.
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Baertsch, N. A., and T. L. Baker-Herman. "Inactivity-induced phrenic and hypoglossal motor facilitation are differentially expressed following intermittent vs. sustained neural apnea." Journal of Applied Physiology 114, no. 10 (May 15, 2013): 1388–95. http://dx.doi.org/10.1152/japplphysiol.00018.2013.
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Reduced respiratory neural activity elicits a rebound increase in phrenic and hypoglossal motor output known as inactivity-induced phrenic and hypoglossal motor facilitation (iPMF and iHMF, respectively). We hypothesized that, similar to other forms of respiratory plasticity, iPMF and iHMF are pattern sensitive. Central respiratory neural activity was reversibly reduced in ventilated rats by hyperventilating below the CO2 apneic threshold to create brief intermittent neural apneas (5, ∼1.5 min each, separated by 5 min), a single brief massed neural apnea (7.5 min), or a single prolonged neural apnea (30 min). Upon restoration of respiratory neural activity, long-lasting (>60 min) iPMF was apparent following brief intermittent and prolonged, but not brief massed, neural apnea. Further, brief intermittent and prolonged neural apnea elicited an increase in the maximum phrenic response to high CO2, suggesting that iPMF is associated with an increase in phrenic dynamic range. By contrast, only prolonged neural apnea elicited iHMF, which was transient in duration (<15 min). Intermittent, massed, and prolonged neural apnea all elicited a modest transient facilitation of respiratory frequency. These results indicate that iPMF, but not iHMF, is pattern sensitive, and that the response to respiratory neural inactivity is motor pool specific.
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Baković, Darija, Davor Eterović, Zoran Valic, Žana Saratlija-Novaković, Ivan Palada, Ante Obad, and Željko Dujić. "Increased pulmonary vascular resistance and reduced stroke volume in association with CO2retention and inferior vena cava dilatation." Journal of Applied Physiology 101, no. 3 (September 2006): 866–72. http://dx.doi.org/10.1152/japplphysiol.00759.2005.
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Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO2and O2were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO2increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (∼4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO2retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.
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Delacourt, C., E. Canet, and M. A. Bureau. "Predominant role of peripheral chemoreceptors in the termination of apnea in maturing newborn lambs." Journal of Applied Physiology 80, no. 3 (March 1, 1996): 892–98. http://dx.doi.org/10.1152/jappl.1996.80.3.892.
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Apneas are very common and normal in newborns but may become life threatening if they are not terminated appropriately. The aim of this study in newborn lambs was to investigate the influence on apnea termination of postnatal maturation, peripheral chemoreceptor function, and hypoxia. Apneas were induced by passive hyperventilation at varying inspired O2 fraction levels. The apnea termination threshold PCO2 (PATTCO2) was defined as the arterial PCO2 value at the first breath after the apnea. Three groups of awake intubated lambs were studied: 1) intact lambs tested at both 1 and 15 days of life, 2) intact 1-day-old lambs with central tissue hypoxia induced by CO inhalation, and 3) 1-day-old lambs with carotid body denervation (CBD). In individual lambs and regardless of age and carotid body function, there was a PO2-PCO2 response curve that was a determinant for the termination of an apnea. PATTCO2 invariably increased when arterial PO2 increased, regardless of age. During hypoxia and normoxia, PATTCO2 was significantly lower in 15-day-old lambs compared with 1-day-old lambs. No difference was seen during hyperoxia. PATTCO2 values were shifted to higher levels after carotid body removal. Finally, hypoxia induced by either a low inspired O2 fraction or CO inhalation consistently failed to induce a depressive effect on the PATTCO2 even in CBD lambs. In conclusion, in awake newborn lambs, the PCO2 level for apnea termination changed with postnatal age, and carotid body function was essential in lowering PATTCO2, thus protecting the lambs against prolonged apnea. Furthermore, hypoxia consistently failed to depress the reinitiation of breathing after apnea, even in CBD lambs.
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Bird, Jordan, Jason Chan, Alexander Rimke, Anne Kalker, Garrick Chan, Tom Brutsaert, Mingma Sherpa, and Trevor Day. "060 Challenging the current assessment criteria for scoring central sleep apnea at altitude." Sleep 44, Supplement_2 (May 1, 2021): A25. http://dx.doi.org/10.1093/sleep/zsab072.059.
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Abstract Introduction Sleep disordered breathing comes in two forms: obstructive and central sleep apnea (SA). Obstructive sleep apnea (OSA) is caused by upper airway collapse during sleep, and is associated with increases in morbidity and mortality. Conversely, central sleep apnea (CSA) results from increases in respiratory chemosensitivity to blood gas challenges in the context of high-altitude ascent. CSA increases in severity and apneas shorten in duration with higher ascent and/or time spent at altitude. Although both types of SA are characterized by intermittent periods of apnea and hyperventilation, the underlying mechanisms and phenotypes between OSA and CSA are different. A universal scoring system for the two types of context-dependent SA may lead to errors in quantification. The American Association of Sleep Medicine (AASM) developed assessment criteria for SA, which are universally-utilized for all types of SA to quantify an apnea-hypopnea index (AHI; events/hour), where apneas are scored as cessation of breathing ≥10-sec. We aimed to assess the effect of reducing the apnea-detection threshold (ADT) to <10-sec to quantitatively assess the extent that a shorter ADT affects the scoring of AHI in the context of high-altitude ascent, where CSA is universal. Methods We assessed CSA using portable polysomnography (ApneaLink, ResMed) during ascent to 5160m in the Nepal Himalaya over 10 days in 15 healthy participants. Files were archived digitally for later analysis using automated scoring software (ApneaLink Reporting Software, ResMed). We quantified and compared AHI using AASM criteria (i.e., 10-sec ADT) and a shorter 5-sec ADT. Results AHI was 3.9±4.1 events/hour at 1045m prior to ascent, with AHI increasing to 37.5±32.8 events/hour (P<0.0001) at 5160m after 10 days of incremental ascent using AASM criteria (i.e., 10-sec ADT). When the ADT was reduced to 5-sec at 5160m, AHI was increased to 61.6±38.1 (+61%; P=0.0002). Conclusion This preliminary report suggests that the AASM criterion for scoring apneas, which is broadly applied to OSA at low altitude, may underestimate the assessment and quantification of CSA with ascent to and prolonged stays at high altitude. Development of distinct assessment criteria for OSA and CSA may be warranted. Support (if any) Natural Science sand Engineering Research Council of Canada
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Siljehav, Veronica, Yuri Shvarev, and Eric Herlenius. "Il-1β and prostaglandin E2 attenuate the hypercapnic as well as the hypoxic respiratory response via prostaglandin E receptor type 3 in neonatal mice." Journal of Applied Physiology 117, no. 9 (November 1, 2014): 1027–36. http://dx.doi.org/10.1152/japplphysiol.00542.2014.
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Prostaglandin E2 (PGE2) serves as a critical mediator of hypoxia, infection, and apnea in term and preterm babies. We hypothesized that the prostaglandin E receptor type 3 (EP3R) is the receptor responsible for PGE2-induced apneas. Plethysmographic recordings revealed that IL-1β (ip) attenuated the hypercapnic response in C57BL/6J wild-type (WT) but not in neonatal (P9) EP3R−/− mice ( P < 0.05). The hypercapnic responses in brain stem spinal cord en bloc preparations also differed depending on EP3R expression whereby the response was attenuated in EP3R−/− preparations ( P < 0.05). After severe hypoxic exposure in vivo, IL-1β prolonged time to autoresuscitation in WT but not in EP3R−/− mice. Moreover, during severe hypoxic stress EP3R−/− mice had an increased gasping duration ( P < 0.01) as well as number of gasps ( P < 0.01), irrespective of intraperitoneal treatment, compared with WT mice. Furthermore, EP3R−/− mice exhibited longer hyperpneic breathing efforts when exposed to severe hypoxia ( P < 0.01). This was then followed by a longer period of secondary apnea before autoresuscitation occurred in EP3R−/− mice ( P < 0.05). In vitro, EP3R−/− brain stem spinal cord preparations had a prolonged respiratory burst activity during severe hypoxia accompanied by a prolonged neuronal arrest during recovery in oxygenated medium ( P < 0.05). In conclusion, PGE2 exerts its effects on respiration via EP3R activation that attenuates the respiratory response to hypercapnia as well as severe hypoxia. Modulation of the EP3R may serve as a potential therapeutic target for treatment of inflammatory and hypoxic-induced detrimental apneas and respiratory disorders in neonates.
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Xu, Fadi, Qi-Hai Gu, Tongrong Zhou, and Lu-Yuan Lee. "Acute hypoxia prolongs the apnea induced by right atrial injection of capsaicin." Journal of Applied Physiology 94, no. 4 (April 1, 2003): 1446–54. http://dx.doi.org/10.1152/japplphysiol.00767.2002.
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Inspiratory central drive is augmented by acute hypoxia that leads to a hyperventilation, but it is inhibited by capsaicin (Cap)-induced stimulation of pulmonary C fibers (PCFs) that produces an expiratory apnea. We hypothesized that acute hypoxia should shorten or eliminate the Cap-induced apnea. The ventilatory responses to bolus injection of Cap (0.2–0.5 μg) into the right atrium before and during acute hypoxia (10% O2 for ∼1 min; Hypoxia+Cap) were compared in anesthetized and spontaneously breathing rats. We found that Cap injection during acute hypoxia produced an extremely long-lasting apnea (69.67 ± 11.97 s) that was 16-fold longer than the apnea induced by Cap alone (expiratory duration = 4.37 ± 0.53 s; P< 0.01). A similar prolonged apnea was also observed during hypoxia in anesthetized guinea pigs. Bilateral vagotomy abolished apneic responses to Cap both before and during hypoxia. Subsequent recording of single-fiber activity of PCFs (PCFA) showed that acute hypoxia did not significantly affect baseline PCFA but that it doubled PCFA responses to Cap via increasing both the firing rate (3.34 ± 0.76 to 7.65 ± 1.32 impulses/s; P < 0.05) and burst duration (1.12 ± 0.18 to 2.32 ± 0.31 s; P < 0.05). These results suggest that acute hypoxia augments PCF-mediated inspiratory inhibition and thereby leads to an extremely long-lasting apnea. This interaction is partially due to hypoxic sensitization of PCF response to Cap.
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Zhang, Gerui, Lin Luo, Limin Zhang, and Zhuo Liu. "Research Progress of Respiratory Disease and Idiopathic Pulmonary Fibrosis Based on Artificial Intelligence." Diagnostics 13, no. 3 (January 18, 2023): 357. http://dx.doi.org/10.3390/diagnostics13030357.
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Machine Learning (ML) is an algorithm based on big data, which learns patterns from the previously observed data through classifying, predicting, and optimizing to accomplish specific tasks. In recent years, there has been rapid development in the field of ML in medicine, including lung imaging analysis, intensive medical monitoring, mechanical ventilation, and there is need for intubation etiology prediction evaluation, pulmonary function evaluation and prediction, obstructive sleep apnea, such as biological information monitoring and so on. ML can have good performance and is a great potential tool, especially in the imaging diagnosis of interstitial lung disease. Idiopathic pulmonary fibrosis (IPF) is a major problem in the treatment of respiratory diseases, due to the abnormal proliferation of fibroblasts, leading to lung tissue destruction. The diagnosis mainly depends on the early detection of imaging and early treatment, which can effectively prolong the life of patients. If the computer can be used to assist the examination results related to the effects of fibrosis, a timely diagnosis of such diseases will be of great value to both doctors and patients. We also previously proposed a machine learning algorithm model that can play a good clinical guiding role in early imaging prediction of idiopathic pulmonary fibrosis. At present, AI and machine learning have great potential and ability to transform many aspects of respiratory medicine and are the focus and hotspot of research. AI needs to become an invisible, seamless, and impartial auxiliary tool to help patients and doctors make better decisions in an efficient, effective, and acceptable way. The purpose of this paper is to review the current application of machine learning in various aspects of respiratory diseases, with the hope to provide some help and guidance for clinicians when applying algorithm models.
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Wickerts, Liselott, Sune Forsberg, Frederic Bouvier, and Jan G. Jakobsson. "Monitoring respiration and oxygen saturation in patients during the first night after elective bariatric surgery: A cohort study." F1000Research 6 (May 22, 2017): 735. http://dx.doi.org/10.12688/f1000research.11519.1.
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Background: Obstructive sleep apnoea and obese hypoventilation is not uncommon in patients with obesity. Residuals effect from surgery/anaesthesia and opioid analgesics may worsen respiration during the first nights after bariatric surgery. The aim of this observational study was to monitor respiration on the first postoperative night following elective bariatric surgery. Methods: This observational study aimed to determine the incidence and severity of hypo/apnea. Oxygen desaturation was analysed by continuous respiratory monitoring. Results: 45 patients were monitored with portable polygraphy equipment (Embletta, ResMed) during the first postoperative night at the general ward following elective laparoscopic bariatric surgery. Mean SpO2 was 93%; 10 patients had a mean SpO2 of less than 92% and 4 of less than 90%. The lowest mean SpO2 was 87%. There were 16 patients with a nadir SpO2 of less than 85%, lowest nadir SpO2 being 63%. An Apnoea Hypo/apnea Index (AHI) > 5 was found in 2 patients only (AHI 10 and 6), and an Oxygen Desaturation index (ODI) > 5 was found in 3 patients (24, 10 and 6, respectively). 3 patients had more prolonged (> 30 seconds) apnoea with nadir SpO2 81%, 83% and 86%. Conclusions: A low mean SpO2 and short episodes of desaturation were not uncommon during the first postoperative night following elective bariatric surgery in patients without history of night time breathing disturbance. AHI and/or ODI of more than 5 were only rarely seen. Night-time respiration monitoring provided sparse additional information. Thus, it seems reasonable to have low risk patients at general ward already in their first night after bariatric surgery.
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Baertsch, Nathan A., and Tracy L. Baker-Herman. "Intermittent reductions in respiratory neural activity elicit spinal TNF-α-independent, atypical PKC-dependent inactivity-induced phrenic motor facilitation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 8 (April 15, 2015): R700—R707. http://dx.doi.org/10.1152/ajpregu.00359.2014.
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In many neural networks, mechanisms of compensatory plasticity respond to prolonged reductions in neural activity by increasing cellular excitability or synaptic strength. In the respiratory control system, a prolonged reduction in synaptic inputs to the phrenic motor pool elicits a TNF-α- and atypical PKC-dependent form of spinal plasticity known as inactivity-induced phrenic motor facilitation (iPMF). Although iPMF may be elicited by a prolonged reduction in respiratory neural activity, iPMF is more efficiently induced when reduced respiratory neural activity (neural apnea) occurs intermittently. Mechanisms giving rise to iPMF following intermittent neural apnea are unknown. The purpose of this study was to test the hypothesis that iPMF following intermittent reductions in respiratory neural activity requires spinal TNF-α and aPKC. Phrenic motor output was recorded in anesthetized and ventilated rats exposed to brief intermittent (5, ∼1.25 min), brief sustained (∼6.25 min), or prolonged sustained (30 min) neural apnea. iPMF was elicited following brief intermittent and prolonged sustained neural apnea, but not following brief sustained neural apnea. Unlike iPMF following prolonged neural apnea, spinal TNF-α was not required to initiate iPMF during intermittent neural apnea; however, aPKC was still required for its stabilization. These results suggest that different patterns of respiratory neural activity induce iPMF through distinct cellular mechanisms but ultimately converge on a similar downstream pathway. Understanding the diverse cellular mechanisms that give rise to inactivity-induced respiratory plasticity may lead to development of novel therapeutic strategies to treat devastating respiratory control disorders when endogenous compensatory mechanisms fail.
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Nattanmai, Premkumar, Christopher R. Newey, Ishpreet Singh, and Keerthivaas Premkumar. "Prolonged duration of apnea test during brain death examination in a case of intraparenchymal hemorrhage." SAGE Open Medical Case Reports 5 (January 1, 2017): 2050313X1771605. http://dx.doi.org/10.1177/2050313x17716050.
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Objective: Apnea test is required as part of the brain death examination. The duration of the apnea test is variable but typically requires 8–10 min. Prolonged apnea tests have been reported in the setting of hypothermia. Here, we describe a case of prolonged duration of apnea test secondary to a phenomenon called cardiac ventilation. Methods: The patient presented in coma with brainstem areflexia after having an intracerebral hemorrhage resulting in subfalcine, central, uncal, and tonsillar herniations. Confounding variables were excluded. Brain death testing was performed, and she was found to have brainstem areflexia. Pre-requisites for apnea test were then met. Results: Apnea testing, however, was prolonged at 110 min. When reconnected to ventilator, it was noted that she had small (30–35 cc) tidal volumes at a rate of her heart rate without respiratory effort. Ancillary testing with four-vessel cerebral angiogram confirmed cerebral circulatory arrest. Conclusions: To our knowledge, this is the longest reported case of apnea testing during brain death testing. Variables known to cause a delay in the rise of carbon dioxide (PaCO2) levels were excluded. We suspect the hyperdynamic cardiac state caused cardiac ventilations resulting in slow increase in carbon dioxide levels.
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Woodson, Gayle E., and George Brauel. "Arterial chemoreceptor influences on the laryngeal chemoreflex." Otolaryngology–Head and Neck Surgery 107, no. 6_part_1 (December 1992): 775–82. http://dx.doi.org/10.1177/019459988910700612.1.
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Prolonged apnea and cardiovascular changes have been elicited in infant animals by the application of water to the laryngeal mucosa. Previous reports have produced conflicting evidence in regard to the possible role of arterial chemoreceptors in modulating this reflex. The present study was designed to determine the effect of carotid body stimulation or suppression on the duration of apnea and severity of cardiovascular changes in response to water in the larynx of piglets. The role of swallowing in terminating the apnea was also Investigated. Hypoxia and isoproterenol, both carotid body stimuli, caused decreased apnea duration. Hyperoxia was associated with prolonged apnea duration; however, dopamine, which inhibits carotid body chemoreceptors, produced no significant change. Hypotension and bradycardia were only observed after prolonged apnea or chemoreceptor stimulation, supporting the concept that the cardiovascular component of the laryngeal chemoreflex is a result of changes in blood gas concentration rather than a direct response to laryngeal chemostimulatlon. The Interval between water application and Initiation of swallowing was not significantly affected by hypoxia or carotid body stimulation and swallowing did not always occur before resumption of breathing.
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Petrova, N. A., I. V. Dobrodeeva, N. P. Shabalov, O. Ivanov, V. V. Petrenko, N. S. Kiseleva, and T. V. Mamaeva. "APNEA IN INFANTS WITH BRONCHOPULMONARY DYSPLASIA DEPENDING ON ITS SEVERITY." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 19, no. 4 (August 28, 2013): 348–55. http://dx.doi.org/10.18705/1607-419x-2013-19-4-348-355.
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Objective. To evaluate bronchopulmonary dysplasia (BPD) impact on apnea incidence and characteristics in infants.Design and methods. We performed cardiorespiratory monitoring in 25 premature infants with BPD and 25 non-BPD preterms comparable in gestational age (26–30 weeks) at ages of less than 29 days, 29–50 days and > 50 days. Results. Infants with moderate to severe BPD tended to have higher apnea incidence when older than 50 days, and more obstructive episodes, compared to infants with mild BPD and without BPD. Infants with mild BPD had similar apnea type ratio as non-BPD infants. In the second and third age intervals, infants with moderate to severe BPD demonstrated similar prolonged apnea incidence but had rather more apnea accompanied by oxygen saturation (SрO2) falls ≤ 80 %, compared to infants with mild BPD and without BPD. During the irst month infants with mild BPD demonstrated shorter apnea episodes, less prolonged apnea and more apnea with SрO2≤80 % falls compared to non-BPD infants. During the second age interval these characteristics did not differ between the groups. Conclusion. Infants with moderate to severe BPD had longer apnea persistence, more signiicant SрO2falls due to apnea. Respiratory control characteristics seem to be comparable in mild BPD and non-BPD infants from the second month of age.
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Defabjanis, Patrizia. "Impact of nasal airway obstruction on dentofacial development and sleep disturbances in children: preliminary notes." Journal of Clinical Pediatric Dentistry 27, no. 2 (January 1, 2004): 95–100. http://dx.doi.org/10.17796/jcpd.27.2.27934221l1846711.
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Respiratory disorders in the upper respiratory tract during sleep are most often part of a continuous pathological process of long standing. Schematically, three clinical syndromes with increasing severity are described: breathing with the mouth open, snoring and sleep apneal hypopnea syndrome. Obstructive sleep apnea syndrome (OSAS) is a subtle, but severe sleep disorder of early childhood. It is often difficult to detect and may have long-term consequences, including failure to thrive, behavioral disturbances, developmental delay, and cor pulmonale.1 These conditions always include a functional maxillofacial perturbation, which may be associated with a constitutional or acquired morphological disorder. Pediatric dentists must be aware of the problems connected with mouth breathing and OSAS (obstructive sleep apnea syndrome) in children as any delay in diagnosis and treatment may cause prolonged morbidity. They also have a role in the diagnosis and co-management of these patients because the signs and symptoms may be recognizable in the dental practice. Besides the medical approach itself, the treatment sometimes is surgical, always orthopedic: the earlier it is initiated, the more effective, simple and unrestraining it is. The aim of this work is to focus attention on the early diagnosis and prevention of these pathologies. Diagnostic guidelines will be illustrated.
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Shenoy, Shanti, Hai Chen, and Elias Karroum. "835 Ictal Central Apneic Events Detected on Polysomnogram: An Educational Case Report." Sleep 44, Supplement_2 (May 1, 2021): A325. http://dx.doi.org/10.1093/sleep/zsab072.832.
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Abstract Introduction Ictal central apneas (ICA) are frequently observed in focal epilepsy, mostly with temporal lobe seizures, and have been considered as potential biomarkers of sudden unexpected death in epilepsy (SUDEP), particularly when they are prolonged and associated with significant hypoxemia. We present an interesting educational case report of occurrence of such ictal apneic events as recorded during a nocturnal diagnostic polysomnogram (PSG). Report of case(s) A 39-year-old woman with history of left focal epilepsy, hypertension, and headaches was referred to the sleep clinic for loud snoring, witnessed apneic events, and excessive daytime sleepiness. She subsequently underwent a diagnostic (PSG) that demonstrated severe obstructive sleep apnea (apnea-hypopnea index of 63.1) associated with significant hypoxemia (nadir SpO2 of 58%). In addition, the patient had one ictal discharge detected on the PSG’s limited electroencephalogram that occurred in N2 sleep and lasted for almost three minutes with a focal onset and progression in the left hemisphere. The ictal discharge was briefly preceded by central apneic events that continued to occur during and shortly after the termination of the ictal discharge. These ICA events were associated with severe oxygen desaturations down to an SpO2 of 62%. The only time during the PSG recording that the patient had central apneic events was around the ictal event. There were no behavior changes on the video during the seizure, but the ictal discharge was associated with a sustained increase in the mentalis muscles activity and a brief tachycardia. The patient’s neurologist was alerted about the above findings on PSG. The patient was taking a lower dose then prescribed of her anti-epileptic medication (topiramate) that was adjusted, and the patient was counseled on the risks associated with the above findings and positive airway pressure therapy was recommended for her severe sleep apnea. Conclusion The above case report illustrates the importance of polysomnography (specifically the recording of respiratory variables rarely performed in epilepsy monitoring units) in the evaluation of patients with epilepsy given that central apneic events (ICA and post-convulsive central apneas) potentially underlie SUDEP, the most common cause of mortality in refractory epilepsy patients and usually occurring during sleep. Support (if any) None
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Donnelly, D. F., and G. G. Haddad. "Prolonged apnea and impaired survival in piglets after sinus and aortic nerve section." Journal of Applied Physiology 68, no. 3 (March 1, 1990): 1048–52. http://dx.doi.org/10.1152/jappl.1990.68.3.1048.
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We examined the effects of carotid body denervation (CX, n = 9), CX + aortic nerve section (CAX, n = 9), and sham surgery (SHAM, n = 7) on cardiorespiratory and metabolic function in young piglets (less than 9 days). For comparison, 1-mo-old pigs were also studied. Studies were performed 1 day after surgery, during which time ventilation (barometric plethysmography), heart rate, blood pressure, arterial blood gases, and electroencephalogram were recorded under normoxia. CX and CAX piglets hypoventilated (arterial PCO2 = 47.1 +/- 2.6 and 45.4 +/- 3.1 Torr, respectively) compared with SHAM piglets (arterial PCO2 = 36.4 +/- 1.5 Torr). CX piglets had an average of 8.0 +/- 3.0 apneas/h, lasting, on average, 26 +/- 3 s. CAX piglets averaged 17.2 +/- 7.9 apneas/h, lasting 30 +/- 5 s. Such long apneas were never observed in SHAM animals. Mean heart rate and blood pressure in denervated piglets were not significantly different from those in SHAM piglets. In animals followed up poststudy, significantly high mortality was observed in CX (5 of 9) and CAX (6 of 9) piglets by 7 days after surgery but not in SHAM animals (0 of 7) despite identical environmental and feed conditions (P less than 0.05; chi 2). One-month-old denervated animals showed periodic breathing and hypoventilation, but none died. These results suggest that in the newborn piglet 1) peripheral chemoreceptors have an active role in maintaining normal ventilation and avoidance of prolonged apnea and 2) survivability in early life is critically dependent on peripheral chemoreceptors.
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Pickens, D. L., G. L. Schefft, and B. T. Thach. "Pharyngeal fluid clearance and aspiration preventive mechanisms in sleeping infants." Journal of Applied Physiology 66, no. 3 (March 1, 1989): 1164–71. http://dx.doi.org/10.1152/jappl.1989.66.3.1164.
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We sought to characterize ventilatory and airway protective responses to pharyngeal stimulation in young infants during sleep. We studied the various responses with respect to frequency of occurrence, effect of increased stimulus intensity, and relation of stimulus fluid to laryngeal structures. Two groups of infants were studied: healthy full-term infants (n = 5) and preterm infants with a history of prolonged apnea (n = 9). We used a nasopharyngeal catheter to deliver small boluses of warm saline (0.02–0.35 ml) to the oropharynx. Responses repeatedly observed in both infant groups included swallows, obstructed respiratory efforts, brief apnea, prolonged apnea, and cough. In both infant groups, swallows and obstructed breaths occurred frequently and cough and prolonged apnea infrequently. The functional significance of some response patterns was clear, whereas that of others was obscure. Larger stimulus volumes yielded more frequent responses (P less than 0.01), and preterm infants responded much more frequently than full-term infants (P less than 0.01). Prolonged apnea was a composite of the other responses and was much more common in preterm than full-term infants (P less than 0.01). The stimulus technique was performed under direct visualization of the airway in two deceased infants. The findings suggested that the relation of the piriform fossae to the interarytenoid notch is important in determining response frequency. Implications for regulation of the removal of upper airway secretions during sleep are discussed.
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Andersson, Johan P. A., Mats H. Linér, and Henrik Jönsson. "Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations." Journal of Applied Physiology 107, no. 3 (September 2009): 809–15. http://dx.doi.org/10.1152/japplphysiol.91434.2008.
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The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., “static apnea” (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with PaO2 and PaCO2 reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 μg/l at the start of apnea to 0.083 μg/l after the apnea ( P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.
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O’Halloran, K. D., J. K. Herman, and G. E. Bisgard. "Differential effects of clonidine on upper airway abductor and adductor muscle activity in awake goats." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 590–97. http://dx.doi.org/10.1152/jappl.1999.87.2.590.
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The purpose of this study was to determine the extent to which α2-adrenoceptor (α2-AR) pathways affect the central motor output to upper airway muscles that regulate airflow. Electromyogram (EMG) measurements were made from posterior cricoarytenoid (PCA), cricothyroid (CT), thyroarytenoid (TA), and middle (MPC) and inferior (IPC) pharyngeal constrictor muscles in awake standing goats. Systemic administration of the α2-AR agonist clonidine induced a highly dysrhythmic pattern of ventilation in all animals that was characterized by alternating episodes of tachypnea and slow irregular breathing patterns, including prolonged and variable expiratory time intervals. Periods of apnea were commonly observed. Dysrhythmic ventilatory patterns induced by clonidine were associated with differential recruitment of upper airway muscles. α2-AR stimulation preferentially decreased the activity of the PCA, CT, and IPC muscles while increasing TA and MPC EMG activities. Clonidine-induced apneas were associated with continuous tonic activation of laryngeal (TA) and pharyngeal (MPC) adductors, leading to airway closure and arterial oxygen desaturation. Tonic activation of the TA and MPC muscles was interrupted only during the first inspiratory efforts after central apnea. Laryngeal abductor, diaphragm, and transversus abdominis EMG activities were completely silenced during apneic events. Ventilatory and EMG effects were reversed by selective α2-AR blockade with SKF-86466. The results demonstrate that α2-AR pathways are important modulators of central respiratory motor outputs to the upper airway muscles.
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Baertsch, Nathan A., and Tracy L. Baker. "Intermittent apnea elicits inactivity-induced phrenic motor facilitation via a retinoic acid- and protein synthesis-dependent pathway." Journal of Neurophysiology 118, no. 5 (November 1, 2017): 2702–10. http://dx.doi.org/10.1152/jn.00212.2017.
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Respiratory motoneuron pools must provide rhythmic inspiratory drive that is robust and reliable, yet dynamic enough to respond to respiratory challenges. One form of plasticity that is hypothesized to contribute to motor output stability by sensing and responding to inadequate respiratory neural activity is inactivity-induced phrenic motor facilitation (iPMF), an increase in inspiratory output triggered by a reduction in phrenic synaptic inputs. Evidence suggests that mechanisms giving rise to iPMF differ depending on the pattern of reduced respiratory neural activity (i.e., neural apnea). A prolonged neural apnea elicits iPMF via a spinal TNF-α-induced increase in atypical PKC activity, but little is known regarding mechanisms that elicit iPMF following intermittent neural apnea. We tested the hypothesis that iPMF triggered by intermittent neural apnea requires retinoic acid and protein synthesis. Phrenic nerve activity was recorded in urethane-anesthetized and -ventilated rats treated intrathecally with an inhibitor of retinoic acid synthesis (4-diethlyaminobenzaldehyde, DEAB), a protein synthesis inhibitor (emetine), or vehicle (artificial cerebrospinal fluid) before intermittent (5 episodes, ~1.25 min each) or prolonged (30 min) neural apnea. Both DEAB and emetine abolished iPMF elicited by intermittent neural apnea but had no effect on iPMF elicited by a prolonged neural apnea. Thus different patterns of reduced respiratory neural activity elicit phenotypically similar iPMF via distinct spinal mechanisms. Understanding mechanisms that allow respiratory motoneurons to dynamically tune their output may have important implications in the context of respiratory control disorders that involve varied patterns of reduced respiratory neural activity, such as central sleep apnea and spinal cord injury. NEW & NOTEWORTHY We identify spinal retinoic acid and protein synthesis as critical components in the cellular cascade whereby repetitive reductions in respiratory neural activity elicit rebound increases in phrenic inspiratory activity.
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Haider, A. Z., V. Rehan, S. Al-Saedi, R. Alvaro, K. Kwiatkowski, D. Cates, and H. Rigatto. "Effect of baseline oxygenation on the ventilatory response to inhaled 100% oxygen in preterm infants." Journal of Applied Physiology 79, no. 6 (December 1, 1995): 2101–5. http://dx.doi.org/10.1152/jappl.1995.79.6.2101.
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We tested the hypothesis that the immediate (< 1 min) ventilatory response to 100% O2 in preterm infants, a test of peripheral chemoreceptor activity characterized by a decrease in ventilation due to apnea, is more pronounced at lower baseline O2 concentrations. We studied 12 healthy preterm infants [birth weight 1,425 +/- 103 (SE) g; study weight 1,670 +/- 93 g; gestational age 30 +/- 1 wk; postnatal age 27 +/- 7 days] during quiet sleep. The infants inhaled 15, 21, 25, 30, 35, 40, and 45% O2 for 5 min in a randomized manner (control period), followed by 100% O2 for 2 min, and then the same initial O2 concentration again for 2 min (recovery period). A nose piece and a flow-through system were used to measure ventilation. The immediate decrease in ventilation with 100% O2 was 46% on 15% O2, 24% on 21% O2, 11% on 25% O2, 8% on 30% O2, 12% on 35% O2, and 8% on 40% O2; there was no decrease on 45% O2 (P < 0.01). The corresponding mean duration of apnea was 29 s during 15% O2, 18 s during 21% O2, 8 s during 25% O2, 9 s during 30 and 35% O2, and 3 s during 40% O2; only one infant developed a 5-s apnea during 45% O2 (P < 0.001). The findings suggest that 1) the ventilatory decrease in response to 100% O2 is dependent on the baseline oxygenation, being more pronounced the lower the baseline O2 concentration; and 2) this ventilatory decrease is entirely related to more prolonged apneas observed with lower baseline O2 concentrations. We speculate that the peripheral chemoreceptors, being so active in the small preterm infant with relatively low arterial PO2, are highly susceptible to changes in PO2, and this makes them prone to irregular or periodic breathing, especially during sleep.
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Peng, Wenhong, Jianguo Zhuang, Kevin S. Harrod, and Fadi Xu. "Respiratory syncytial virus infection in anesthetized weanling rather than adult rats prolongs the apneic responses to right atrial injection of capsaicin." Journal of Applied Physiology 102, no. 6 (June 2007): 2201–6. http://dx.doi.org/10.1152/japplphysiol.01436.2006.
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Apnea is a common complication in infants infected by respiratory syncytial virus (RSV). A recent study has shown that intranasal inoculation of RSV in conscious weanling rats strengthens the apneic responses to right atrial injection of capsaicin (CAP), leading to 66% mortality. The objectives of the present study were to determine 1) whether RSV infection changes baseline minute ventilation (V̇e) and arterial blood gases in anesthetized rats; 2) what the effects of RSV infection are on the respiratory responses to CAP; and 3) whether the RSV-strengthened apneic responses are age dependent. Our experiments were conducted in anesthetized and spontaneously breathing rats divided into four groups of weanling and adult rats that received either intranasal inoculation of RSV or virus-free medium. Two days after RSV infection (0.7 ml/kg), animal blood gases, baseline V̇e, and V̇e responses to right atrial injection of three doses of CAP (4, 16, and 64 μg/kg) were measured and compared among the four groups. Our results showed that RSV infection increased respiratory frequency (∼25%, P < 0.05) in weanling but not adult rats, with little effect on arterial blood gases. RSV infection amplified the apneic responses to CAP in weanling but not adult rats, characterized by increases in the initial (40%) and the longest apneic duration (650%), the number of apneic episodes (139%), and the total duration of apneas (60%). These amplifications led to 50% mortality ( P < 0.05). We conclude that RSV infection increases respiratory frequency and strengthens the apneic responses to CAP only in anesthetized weanling but not adult rats.
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Steinschneider, Alfred, and Vicki Santos. "Parental Reports of Apnea and Bradycardia: Temporal Characteristics and Accuracy." Pediatrics 88, no. 6 (December 1, 1991): 1100–1105. http://dx.doi.org/10.1542/peds.88.6.1100.
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A prospective examination was made of the temporal course of parental observations in response to a monitor alarm of apnea (apnea setting of 20 seconds) or bradycardia (bradycardia setting of 80 beats per minute). Data were obtained from 155 subsequent sudden infant death syndrome siblings followed up at home, during the first 20 weeks of life, on an apnea/bradycardia monitor with an attached event recorder. In addition, parental reports were compared to an objective recording of the pattern of cardiorespiratory activity surrounding each monitor alarm. Only those parental observations were considered which reported the infant to be asleep with no apparent equipment malfunction following an apnea alarm (with or without pallor, cyanosis, or the provision of external stimulation) or a low heart rate alarm associated with pallor, cyanosis, or stimulation. Observations were analyzed within each of five age periods (<29, 29 through 56, 57 through 84, 85 through 112, 113 through 140 days). The percentage of infants reported to have prolonged apnea, prolonged apnea with stimulation, or bradycardia with stimulation was found to decrease with age. An examination of the linked event recordings failed to document an episode of apnea as long as 15 seconds for any of the reported episodes of apnea. Furthermore, bradycardia as long as 5 seconds in duration could be documented in only 3 of 422 reported episodes of bradycardia. These results indicate the potential for considerable error when total reliance is placed on parental observations and point to the necessity for objective event recordings when using home monitors in the clinical management of at-risk infants.
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Davis, Marina R., Jennifer L. Magnusson, and Kevin J. Cummings. "Increased central cholinergic drive contributes to the apneas of serotonin-deficient rat pups during active sleep." Journal of Applied Physiology 126, no. 5 (May 1, 2019): 1175–83. http://dx.doi.org/10.1152/japplphysiol.00909.2018.
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Infant rat pups lacking central nervous system (CNS) serotonin (5-hydroxytryptamine; 5-HT) have unstable breathing during prolonged periods of active sleep. Given that cholinergic neurons are drivers of active sleep and project to respiratory patterning regions in the brainstem, we hypothesized that 5-HT preserves respiratory stability in active sleep by dampening central cholinergic drive. We used whole-body plethysmography coupled with nuchal electromyography to monitor the breathing pattern of 2-wk-old tryptophan hydroxylase 2 ( TPH2)+/+ and TPH2-deficient ( TPH2−/−) pups in active sleep, before and after muscarinic blockade. For the group 1 experiment we injected methylatropine (Ap-M), a CNS-impermeant form of atropine, followed ~30 min later by an injection of atropine sulfate (Ap-S), the CNS-permeant form (both 1 mg/kg, 10 μl bolus iv); both injections occurred within an active sleep episode. We analyzed the effect of each drug on the coefficient of variation of the respiratory period (CV-P) during active sleep. For the group 2 experiment rats were cycled through several episodes of active and quiet sleep before administration of Ap-S (1 mg/kg, 200 μl ip) or vehicle. We assessed the effect of Ap-S on the apnea indices of both genotypes during quiet and active sleep. In group 1 Ap-S significantly reduced the CV-P of TPH2−/− pups ( P = 0.03), an effect not observed in TPH2+/+ pups or following Ap-M. In group 2 the apnea index of TPH2−/− pups was significantly reduced following Ap-S injection ( P = 0.04), whereas the apnea index of TPH2+/+ littermates was unaffected ( P = 0.58). These findings suggest that central 5-HT reduces apnea and stabilizes breathing by reducing cholinergic signaling through muscarinic receptors. NEW & NOTEWORTHY Serotonin in the central nervous system (CNS) is necessary for maintaining the stability of breathing in the early postnatal period, particularly during active sleep. Here we show that the administration of atropine to the CNS selectively stabilizes the respiratory pattern of tryptophan hydroxylase 2-deficient rat pups and reduces their apneas. This suggests that CNS serotonin stabilizes breathing at least in part by reducing central cholinergic drive.
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Grogaard, J., A. Van den Abbeele, and H. Sundell. "Effect of alcohol on apnea reflexes in young lambs." Journal of Applied Physiology 59, no. 2 (August 1, 1985): 420–25. http://dx.doi.org/10.1152/jappl.1985.59.2.420.
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This study examined the effect of alcohol on two apnea reflexes considered to be protective mechanisms through which animals and humans preserve vital functions while they are submerged in water. The laryngeal chemoreflex and the trigeminal diving reflex were studied in unanesthetized 1- to 3-wk-old lambs. Reflex stimulation resulted in reduced ventilation or apnea, bradycardia, hypertension, and blood flow redistribution in the dive pattern. After alcohol, reflex stimulation resulted in increased apnea response, preserved blood flow redistribution, but less hypertension. The onset of regular breathing following laryngeal water stimulation was significantly delayed, after alcohol, and mechanical ventilation was used in three lambs to terminate the prolonged poststimulus apnea. Airway occlusion pressure, an index of neuromuscular inspiratory drive, decreased significantly after alcohol. The study demonstrates a potent effect of alcohol on apnea reflex responses. The effect of alcohol on respiratory drive and on the apnea reflex response should be considered when humans ingest alcohol, in particular by those participating in water sports.
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SOUTHALL, DAVID P. "Cerebrospinal Fluid Endorphins and the Infant Apnea Syndrome." Pediatrics 79, no. 5 (May 1, 1987): 838. http://dx.doi.org/10.1542/peds.79.5.838.
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To the Editor.— In his interesting paper (Pediatrics 1986;78:233-237), Orlowski states that one explanation for elevated levels of endorphins might be that they increase in response to the stress of a prolonged apneic episode. He rightly points out that elevated endorphin levels alone do not demonstrate a causal relationship to prolonged "abnormal" apnea. Unfortunately, he subsequently implied that, because the number of short, normally occurring, apneic pauses of 4 to 10 seconds in the group with high endorphin levels appear to be reduced in frequency by naloxone, this finding supports a primary role for endorphins in the genesis of abnormal apnea.
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Sisniega, Carlos, and Umakanth Katwa. "Children with Upper Airway Dysfunction: At Risk of Obstructive Sleep Apnea." Journal of Child Science 09, no. 01 (January 2019): e59-e67. http://dx.doi.org/10.1055/s-0039-1688956.
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AbstractObstructive sleep apnea is characterized by prolonged partial upper airway obstruction or intermittent complete obstruction that disrupts normal ventilation during sleep and alters normal sleep patterns. Patients with obstructive sleep apnea tend to develop neurocognitive, cardiovascular, behavioral, attention issues, and poor academic performance. Therefore, it is essential to diagnose and treat obstructive sleep apnea early and avoid significant and long-lasting adverse outcomes. Most commonly, upper airway obstruction is caused by enlarged lymphoid tissues within the upper airway, and therefore adenotonsillectomy is considered as the first-line treatment of obstructive sleep apnea in children. Fifty to 70% of patients who have obstructive sleep apnea and treated by surgery are not entirely cured on follow-up polysomnography. In light of this, it is recommended that patients with suspected obstructive sleep apnea undergo a thorough evaluation, and all potential risk factors are identified and treated. The purpose of this review is to familiarize pediatricians with developmental, anatomical, and physiological risk factors involved in the development of obstructive sleep apnea. Additionally, we will present an array of evaluation techniques that can offer adequate assessment of the patient's upper airway anatomy and physiology.
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Steinschneider, Alfred, Vicki Santos, and Gary Freed. "Cost Implications of Event Recordings In Apnea/Bradycardia Home Monitoring: A Theoretical Analysis." Pediatrics 95, no. 3 (March 1, 1995): 378–80. http://dx.doi.org/10.1542/peds.95.3.378.
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Objectives. To evaluate the financial impact of incorporating event recordings as an integral component of home apnea/bradycardia monitoring. Study design. This theoretical analysis examines the cost of home monitoring when medical decisions are based on an evaluation of the cardiorespiratory wave-forms surrounding each apnea/bradycardia monitor alarm (documented monitoring) compared to those based on parental observations. Data for both approaches were obtained from 155 infants referred within the first 10 days of life, because a sibling died of sudden infant death syndrome. All were followed on an impedance type apnea/bradycardia monitor with an attached event recorder. The monitor settings were 20 seconds for apnea and 80 beats per minute (bpm) for bradycardia. Parents were taught how to use the equipment, resuscitative techniques, and to complete an alarm log. The clinical protocol provided for home monitoring until there were no "episodes" (prolonged apnea or prolonged bradycardia) for 16 consecutive weeks. A polysomnogram would be obtained if an "episode" occurred. For each infant two independent approaches were used to judge the occurrence of an "episode": (1) parental report of an apnea alarm occurring during sleep or a physiologic alarm associated with skin color change or resuscitative intervention and (2) apnea ≥ 20 seconds long or bradycardia ≥ 10 seconds. The cost was calculated assuming a 4-week monitor rental fee of $350, a 4-week waveform interpretation fee of $180, and a $600 fee for performing and interpreting a polysomnogram. Results. Episodes defined from an interpretation of the cardiorespiratory waveforms resulted in fewer diagnostic studies, a shorter period of home monitoring, and lower per patient treatment costs. Conclusion. Despite the increased monthly cost, incorporating event recordings as an integral component of home monitoring resulted in a lower average per patient cost.
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CUMMINS, SUSAN K. "Statistics and Sudden Infant Death Syndrome." Pediatrics 79, no. 3 (March 1, 1987): 486–87. http://dx.doi.org/10.1542/peds.79.3.486a.
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To the Editor.— The recent cohort study by Oren et al1 examined risk factors for sudden infant death syndrome (SIDS) in infants with prolonged unexplained sleep apnea with color change (severe apnea of infancy). This analysis revealed three possible risk factors for SIDS death: having a subsequent monitored apnea episode needing resuscitation or vigorous stimulation, being a sibling of a SIDS victim, or developing a seizure disorder after monitoring began. Unfortunately, there are two serious problems with the authors' analysis: the misrepresentation of relative risk and the use of the χ2 statistic to test associations in small subgroups.
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James, Mary, Anuja J. S., and Praveen Jacob Ninan. "Clinical profile of neonatal candidiasis in newborn nursery." International Journal of Contemporary Pediatrics 5, no. 2 (February 22, 2018): 334. http://dx.doi.org/10.18203/2349-3291.ijcp20180034.
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Background: Candidiasis refers to infection with fungi of the genus candida. Candida infections are frequent and major causes of septicemia in neonatal intensive care units and are associated with high morbidity and mortality. Low birth weight preterm infants are especially vulnerable to these devastating infections. Candida infections are a major cause of septicemia in neonatal ICUs and may affect 1.6% to 12.9% of very low birth weight infants. The smaller the infant is, the greater is the likelihood for systemic fungal infection to develop.Methods: 40 Newborns with culture proven candidiasis admitted in new-born nursery of Government T. D Medical College, Alappuzha, were selected for the study. The significance of different parameters such as gender, gestational age, birth weight, Apgar score, duration of hospital stays, central venous catheter and use of third generation cephalosporins were analysed. Clinical profile like apnoea, feed intolerance, requirement of ventilator support, temperature instability, thrombocytopenia, hyperglycemia etc. were analyzed.Results: Out of 40 newborns 39 were preterms, 42% of study population were having a birth weight of 1-1.5 kg, 33% with a birth weight of 1.5-2 kg and 20% with a birth weight of <1 kg.75% of the study population were hospitalized for >1 week. In the study group 58% had feed intolerance, 52.5% needed ventilator support, 52.5% had temperature instability, 70% had thrombocytopenia 50% had apnea and 4% had hyperglycemia. The overall survival was 60%.Conclusions: Prematurity, low birth weight and prolonged hospital stay were associated with increased risk of candidiasis. Feed intolerance, increased need for ventilator support, apnea, temperature instability and thrombocytopenia were significant clinical parameters.
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Fewell, James E., and Francine G. Smith. "Perinatal nicotine exposure impairs ability of newborn rats to autoresuscitate from apnea during hypoxia." Journal of Applied Physiology 85, no. 6 (December 1, 1998): 2066–74. http://dx.doi.org/10.1152/jappl.1998.85.6.2066.
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Failure to autoresuscitate by hypoxic gasping during prolonged sleep apnea has been suggested to play a role in sudden infant death. Furthermore, maternal smoking has been repeatedly shown to be a risk factor for sudden infant death. The present experiments were carried out on newborn rat pups to investigate the influence of perinatal exposure to nicotine (the primary pharmacological and addictive agent in tobacco) on their time to last gasp during a single hypoxic exposure and on their ability to autoresuscitate during repeated exposure to hypoxia. Pregnant rats received either nicotine (6 mg ⋅ kg−1 ⋅ 24 h−1) or vehicle continuously from day 6 of gestation to days 5 or 6 postpartum via an osmotic minipump. On days 5 or 6 postpartum, pups were exposed either to a single period of hypoxia (97% N2-3% CO2) and their time to last gasp was determined, or they were exposed repeatedly to hypoxia and their ability to autoresuscitate from primary apnea was determined. Perinatal exposure to nicotine did not alter the time to last gasp, but it did impair the ability of pups to autoresuscitate from primary apnea. After vehicle, the pups were able to autoresuscitate from 18 ± 1 (SD) periods of hypoxia, whereas, after nicotine, the pups were able to autoresuscitate from only 12 ± 2 periods ( P < 0.001) of hypoxia. Thus our data provide evidence that perinatal exposure to nicotine impairs the ability of newborn rats to autoresuscitate from primary apnea during repeated exposure to hypoxia, such as may occur during episodes of prolonged sleep apnea.
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Garg, Meena, Sharon I. Kurzner, Daisy Bautista, and Thomas G. Keens. "Hypoxic Arousal Responses in Infants With Bronchopulmonary Dysplasia." Pediatrics 82, no. 1 (July 1, 1988): 59–63. http://dx.doi.org/10.1542/peds.82.1.59.
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Infants with bronchopulmonary dysplasia have a high incidence of sudden, unexplained death in the postneonatal period, yet the cause of these deaths is unknown. Frequent episodes of clinically unsuspected arterial oxygen desaturation have recently been described in infants with bronchopulmonary dysplasia. We hypothesized that infants with bronchopulmonary dysplasia who experience frequent episodes of hypoxia may have abnormal arousal responses to these hypoxic episodes. We studied 12 infants with bronchopulmonary dysplasia at 41.4 ± 1.3 weeks postconceptional age. Hypoxic arousal responses were performed during quiet sleep at an inspired oxygen tension of 80 mm Hg for a maximum of three minutes or until arousal occurred. Of 12 infants, 11 (92%) aroused normally to the hypoxic challenge. However, all infants required vigorous stimulation and supplemental oxygen after the initial arousal response. Of 12 infants with bronchopulmonary dysplasia, eight (67%) experienced prolonged apnea with bradycardia, and four of 12 (33%) required brief ventilatory assistance (bag and mask) to restore normal breathing. Abnormal pneumographic findings did not predict the occurrence of these prolonged periods of apnea and bradycardia following hypoxia. We conclude that an abnormal response to hypoxia following arousal may lead to prolonged apnea and bradycardia in infants with bronchopulmonary dysplasia. We speculate that the inability to recover from this hypoxia may result in sudden death in these infants.
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Kianicka, Irenej, Véronique Diaz, Sylvain Renolleau, Emmanuel Canet, and Jean-Paul Praud. "Laryngeal and abdominal muscle electrical activity during periodic breathing in nonsedated lambs." Journal of Applied Physiology 84, no. 2 (February 1, 1998): 669–75. http://dx.doi.org/10.1152/jappl.1998.84.2.669.
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Kianicka, Irenej, Véronique Diaz, Sylvain Renolleau, Emmanuel Canet, and Jean-Paul Praud. Laryngeal and abdominal muscle electrical activity during periodic breathing in nonsedated lambs. J. Appl. Physiol. 84(2): 669–675, 1998.—We recently reported that glottic closure was present throughout central apneas in awake lambs. The present study tested whether glottic closure was also observed during periodic breathing (PB). We attempted to induce PB in 21 nonsedated lambs on return from hypocapnic hypoxia to room air. Airflow and thyroarytenoid (a laryngeal constrictor, n = 16), cricothyroid (a laryngeal dilator, n = 10), and abdominal ( n = 9) muscle electrical activity (EMG) were monitored continuously. PB was observed in 16 lambs, with apneic phases in 8 lambs. Thyroarytenoid muscle EMG was observed at the nadir of PB, either throughout apnea or with prolonged expiration during the lowest respiratory efforts. Phasic inspiratory cricothyroid muscle EMG and phasic expiratory abdominal EMG disappeared at the nadir of PB. Active glottic closure at the nadir of PB, without abdominal muscle contraction, could be a beneficial mechanism, preserving alveolar gas stores for continuing gas exchange during the apneic/hypopneic phase of PB. However, consequences of active glottic closure on ventilatory instability, either enhancing or reducing, are unknown.
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Ma, Cheng, Denisse Broadbent, Garrett Levin, Sanjeet Panda, Devaraj Sambalingam, Norma Garcia, Edson Ruiz, and Ajay Pratap Singh. "Discharging Preterm Infants Home on Caffeine, a Single Center Experience." Children 7, no. 9 (August 28, 2020): 114. http://dx.doi.org/10.3390/children7090114.
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Background: Apnea of prematurity (AOP) affects preterm neonates. AOP, combined with intermittent hypoxemic (IH) events frequently prolongs the length of stay. Caffeine is the preferred medication to treat AOP and may help improve IH events. There is lack of information on the safety of discharging preterm neonates home on caffeine for AOP in the literature. Our objective was to assess safety and benefits, if any, of discharging preterm infants home on caffeine. Methods: After IRB approval, preterm infants discharged home from the neonatal intensive care unit (NICU) on caffeine were compared with those without a discharge prescription for the period of January 2013 to December 2017. Results: A total of 297 infants were started on caffeine, and of those, 87 infants were discharged home on caffeine. There was no difference in length of stay between two groups. Duration of caffeine at home was 31 (28–42) days. The average cost of apnea monitor and caffeine at home per 30 days was USD 1326 and USD 50. There was no difference in number or reasons for emergency department (ED) visits or hospitalizations between two groups. Conclusion: AOP affects almost all preterm infants and along with intermittent hypoxemic events, and is one of the most common reasons for prolonged hospital stay. Discharging stable preterm infants home on caffeine may be safe, especially in those who are otherwise ready to be discharged and are only awaiting complete resolution of AOP/IH events.
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Thompson, Dana M., Michael J. Rutter, J. Paul Willging, Colin D. Rudolph, and Robin T. Cotton. "Altered Laryngeal Sensation: A Potential Cause of Apnea of Infancy." Annals of Otology, Rhinology & Laryngology 114, no. 4 (April 2005): 258–63. http://dx.doi.org/10.1177/000348940511400402.
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Delayed maturation of respiratory control of breathing and the laryngeal adductor reflex (LAR) are commonly implicated in infant apnea. A swallow response occurs to remove the stimulus from the pharynx to prevent aspiration once the glottis reopens. Induction of apnea by poorly cleared endogenous upper airway secretions has been postulated to be a potential cause of infant apnea. Our purpose was to determine whether alteration in the LAR, an indicator of laryngeal sensation, and the presence of secretions influenced the responsiveness of the LAR in infants with apnea. The LAR was induced in 20 infants with apnea (median gestational age, 36.5 weeks) by application of air pulses of controlled duration (50 ms) and intensity (2.5 to 10 mm Hg) to the aryepiglottic fold. Twenty infants evaluated for upper respiratory tract anomalies were used as a comparison group (median gestational age, 39 weeks). The infants with apnea required higher-intensity stimuli (p < .001) to induce the LAR (6.2 ± 1.6 mm Hg) than did the comparison group (4.3 ± 1.0 mm Hg) and demonstrated poorer clearance of secretions (p < .001). These findings were significant even when we adjusted for postconceptional age at the time of the test (p = .007). The findings of this study suggest that decreased laryngeal sensitivity results in poor endogenous secretion clearance and that it may induce a prolonged glottic closure event to prevent aspiration. This closure may play a role in infant apnea.
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Chin, Chien-Hung, Jason P. Kirkness, Susheel P. Patil, Brian M. McGinley, Philip L. Smith, Alan R. Schwartz, and Hartmut Schneider. "Compensatory responses to upper airway obstruction in obese apneic men and women." Journal of Applied Physiology 112, no. 3 (February 1, 2012): 403–10. http://dx.doi.org/10.1152/japplphysiol.00021.2011.
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Defective structural and neural upper airway properties both play a pivotal role in the pathogenesis of obstructive sleep apnea. A more favorable structural upper airway property [pharyngeal critical pressure under hypotonic conditions (passive Pcrit)] has been documented for women. However, the role of sex-related modulation in compensatory responses to upper airway obstruction (UAO), independent of the passive Pcrit, remains unclear. Obese apneic men and women underwent a standard polysomnography and physiological sleep studies to determine sleep apnea severity, passive Pcrit, and compensatory airflow and respiratory timing responses to prolonged periods of UAO. Sixty-two apneic men and women, pairwise matched by passive Pcrit, exhibited similar sleep apnea disease severity during rapid eye movement (REM) sleep, but women had markedly less severe disease during non-REM (NREM) sleep. By further matching men and women by body mass index and age ( n = 24), we found that the lower NREM disease susceptibility in women was associated with an approximately twofold increase in peak inspiratory airflow ( P = 0.003) and inspiratory duty cycle ( P = 0.017) in response to prolonged periods of UAO and an ∼20% lower minute ventilation during baseline unobstructed breathing (ventilatory demand) ( P = 0.027). Thus, during UAO, women compared with men had greater upper airway and respiratory timing responses and a lower ventilatory demand that may account for sex differences in sleep-disordered breathing severity during NREM sleep, independent of upper airway structural properties and sleep apnea severity during REM sleep.
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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Jerome A. Dempsey. "Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep." Journal of Applied Physiology 100, no. 1 (January 2006): 171–77. http://dx.doi.org/10.1152/japplphysiol.00440.2005.
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To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired Po2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O2 saturation = 78–80%), and hyperoxia (inspired O2 fraction = 50–52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 ± 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 ± 0.8 s; P < 0.05), whereas hyperoxia prolonged it (71.5 ± 13.8 s; P < 0.01). The apneic threshold end-tidal Pco2 (PetCO2) was defined as the PetCO2 at the onset of apnea. During hypoxia, the apneic threshold PetCO2 was higher (38.9 ± 1.7 Torr; P < 0.01) compared with normoxia (35.8 ± 1.1; Torr); during hyperoxia, it was lower (33.0 ± 0.8 Torr; P < 0.05). Furthermore, the difference between the eupneic PetCO2 and apneic threshold PetCO2 was smaller during hypoxia (3.0 ± 1.0 Torr P < 001) and greater during hyperoxia (10.6 ± 0.8 Torr; P < 0.05) compared with normoxia (8.0 ± 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO2 below the eupneic PetCO2 was increased by hypoxia (3.44 ± 0.63 l·min−1·Torr−1; P < 0.05) and decreased by hyperoxia (0.63 ± 0.04 l·min−1·Torr−1; P < 0.05) compared with normoxia (0.79 ± 0.05 l·min−1·Torr−1). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors.
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Ovchinnikov, A. Yu, M. A. Edzhe, and M. N. Potemkin. "Application of TruBlue laser light for the treatment of patients with snoring and obstructive sleep apnea syndrome." Laser Medicine 26, no. 1 (July 27, 2022): 24–29. http://dx.doi.org/10.37895/2071-8004-2022-26-1-24-29.
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Purpose: to study the effectiveness of surgical treatment of patients with snoring and obstructive sleep apnea syndrome using TruBlue laser light.Material and methods. Forty patients suffering of snoring and obstructive sleep apnea syndrome were taken into the study. Outcomes of their treatment are described in the present article. All patients had surgical interventions in the volume of uvulopalatoplasty performed with blue TruBlue laser light, wavelength 445 ± 5 nm (main group – 18 patients) and with Surgitron radio wave apparatus (control group – 22 patients). An objective assessment of respiratory disorders during sleep was done with Apnea Link Air respiratory monitoring system; the obtained fi ndings showed that most of the patients in both groups had snoring without apnea (44.4 and 45.4 %); the obstructive sleep apnea syndrome in them was of mild (38.9 and 36.4 %, correspondingly) and of moderate form (16.7 and 18.2 %, correspondingly).Results. Intraoperative blood loss was less in the main group 1 (2.3 ± 1.1 ml) than in the controls (7.1 ± 1.4 ml). In the postoperative period, patients of the main group had less points (7.1 ± 1.4 by the visual-analog scale) and less prolonged pain syndrome (up to 12 days) than in the control group (7.9 ± 1.2 points, up to 14 days). The subjective positive assessment of symptoms (decreased snoring, daytime sleepiness) was registered in both groups. Respiratory monitoring revealed no deterioration in sleep breathing parameters; decreased apnea/hypopnea index was noted in all observations; however, mild obstructive sleep apnea syndrome was detected in patients in both groups (27.8 and 22.7 %) one month after the surgical treatment.Conclusion. TruBlue laser light applied in the snoring and obstructive sleep apnea syndrome has been shown to be effective, causing less pronounced blood loss and pain syndrome, if to compare to the radio wave technique.
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Poets, Christian F., Valerie A. Stebbens, David Richard, and David P. Southall. "Prolonged Episodes of Hypoxemia in Preterm Infants Undetectable by Cardiorespiratory Monitors." Pediatrics 95, no. 6 (June 1, 1995): 860–63. http://dx.doi.org/10.1542/peds.95.6.860.
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Objective. To determine whether episodes of prolonged hypoxemia occur without prolonged apneic pauses (≥20 seconds) and without bradycardia (pulse rate, ≤100 beats per minute) in apparently well preterm infants. Methods. Long-term recordings of arterial oxygen saturation as measured by pulse oximetry (SpO2), photoplethysmographic (pulse) waveforms from the oximeter, and breathing movements were performed in 96 preterm infants (median gestational age at birth, 34 weeks; range, 28 to 36 weeks) who were breathing room air. Recordings started at a median age of 4 days (range, 1 to 60 days). Results. During a median duration of recording of 25 hours, 88 episodes in which SpO2 fell to 80% or less and remained there for 20 seconds or longer were identified in 15 infants. The median duration of these prolonged desaturations was 27 seconds (range, 20 to 81 seconds). In 73 episodes (83%), SpO2 continued to fall to 60% or less. Twenty-three desaturations were associated with prolonged apneic pauses and 54 with bradycardia; 19 of these were associated with both apnea and bradycardia. Thirty desaturations (34%; 10 infants) occurred without bradycardia and without prolonged apnea. Conclusions. These results indicate that a proportion of apparently well preterm infants exhibit episodes of severe prolonged hypoxemia unaccompanied by prolonged apneic pauses or bradycardia. Such episodes, therefore, would be difficult to detect if only breathing movements and heart rate are monitored. Indications for the use of oxygenation monitors in preterm infants should be reconsidered.
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Gaszynski, Tomasz. "Nasal Continuous Positive Airway Pressure During Intubation in Superobese Patients Prolongs Safe Apnea Period." Anesthesia & Analgesia 129, no. 1 (July 2019): e34. http://dx.doi.org/10.1213/ane.0000000000004176.
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Little, Jane A., Seth Rotz, Ceonne Kim, MaryAnn O'Riordan, Nathan Langer, and Colleen Lance. "Nocturnal Hypoxemia (not sleep apnea) May Drive Reticulocytosis in Sickle Cell Disease." Blood 124, no. 21 (December 6, 2014): 1384. http://dx.doi.org/10.1182/blood.v124.21.1384.1384.
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Abstract Introduction: Obstructive sleep apnea is a ventilatory defect that affects up to 10% of children with sickle cell disease (SCD). Sleep apnea has been implicated in cardiovascular disease in non-SCD adults and in cerebrovascular disease in children with SCD. In addition, prolonged hemoglobin oxygen desaturation from sleep disorderedbreathing would be predicted to increase sickle polymer formation and, possibly, activity of disease. We evaluated symptomatic adults from our SCD clinic for sleep apnea, in an effort to identify treatable disease modifying conditions. Methods: 46 adults with SCD were evaluated by polysomnography (PSG) between 2012 and 2014. Subjects were referred for symptoms or signs suggestive of sleep disordered breathing, including nighttime pain, snoring, early morning headache, narrow hypo-pharynx, and/or excessive reticulocytosis. Clinical characteristics of homozygous (HbSS, n=34) and compound heterozygous (HbSC and HbSBeta+Thalassemia, n=12) subjects are shown in Table 1. Results: Sleep apnea was diagnosed if the apnea/hypopnea index (AHI) was elevated: 5-15 (mild), 15-30 (moderate), or >30 (severe). Over half of our patients had sleep apnea by these criteria (16/34 HbSS and 7/12 compound heterozygotes). An elevated 3% oxygen desaturation index , i.e. >15 episodes per hour during which oxygen saturation dropped by 3% or more, was seen in one-third (14/43) of all evaluable subjects, and was 17 (median, range 1.2- 192.4) in subjects with, compared with 4.6 (median, range 1-23.7) in subjects without, sleep apnea (P<.001). Sleep apnea was moderate or severe in 5/34 (14.7%) and 3/12 (25%) of screened HbSS and compound heterozygote patients, respectively. However, the presence of sleep apnea, compared with the absence of sleep apnea, was not associated with differences in measured clinical variables including WBC, Hgb, absolute reticulocyte count, LDH, urinary albumin-to-creatinine ratio, or tricuspid regurgitant jet velocity. We then examined 8 subjects (7 HbSS, 1 SBeta+ thal) whose PSG showed >10% of sleep time afflicted by nocturnal hypoxemia. A median of 33.75% (range 16-98.6%) of sleep time was spent at <90% oxygen saturation in these subjects. Only 3 of 8 subjects with nocturnal hypoxemia had sleep apnea, based on an AHI >5, which was not different than the group as a whole (P=0.7). These 8 subjects had strikingly increased reticulocyte counts, compared with 38 subjects without nocturnal hypoxemia (median 460, range 100-923 (x103)/μL compared with median 303, range 76-733 (x103)/μL respectively, p=0.04), as well as a trend toward a higher LDH (median 488, range 140-752, compared with median 318, range 139-823, P=.08). Of note, hemoglobin levels were not different between subjects with and without nocturnal hypoxemia (mean 8.4±1.5 g/dL compared to mean 9.5±2.2 g/dL, respectively, p=0.17). Conclusions & Discussion: These studies suggest that, while sleep apnea is common in adults with SCD, greater physiological relevance may arise instead from prolonged nocturnal hypoxemia and associated reticulocytosis. We speculate that significant nighttime hypoxemia and hemoglobin desaturation may stimulate both endogenous erythropoietin (and therefore reticulocyte) production and HbS polymer formation and, possibly, hemolysis. This condition, while identifiable by conventional PSG, is not coincident with sleep apnea, and may be modulated by nighttime oxygen supplementation. These findings deserve confirmation in a larger cohort of patients. Table I.Clinical Characteristics of adults with SCD who underwent PolysomnographyHbSS(n=34)Compound Heterozygous (HbSC, n=8, HbSβ+Thal, n=4)P ValueAge (years)27 (19-50)29.5 (19-51)n.s.Body Mass Index23.8 (17.8-37.6)27.2 (20.1-59.8)n.s.Hgb (g/dL, mean±std dev)8.7±1.910.9±2.0P=.003ARC* (x103/μL),350 (93-923)200 (71-398)P=.004LDH (IU/L)398 (149-823)200 (140-632)P<.001TRV**(m/s)2.5 (n.d.-3.51)1.9 (n.d.-2.64)P<.001*Absolute reticulocyte count **Tricuspid regurgitant jet velocity ¦Median with range, unless otherwise indicated. Disclosures No relevant conflicts of interest to declare.
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Palmer, William, Miriam Jaziri, and Maria Tovar. "Positional Therapy in a Patient With Refractory Treatment-Emergent Central Sleep Apnea." Journal of Sleep Medicine 18, no. 3 (December 31, 2021): 182–85. http://dx.doi.org/10.13078/jsm.210019.
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Treatment-emergent central sleep apnea (TE-CSA) is commonly encountered during the treatment for obstructive sleep apnea (OSA) with positive airway pressure (PAP) and usually remains self-limited. Persistent TE-CSA is sporadically seen with PAP therapy and has only rarely been described with hypoglossal nerve stimulation (HGNS). We report the case of a 60-year-old female patient with moderate OSA that progressed to TE-CSA with PAP therapy. A prolonged trial with PAP therapy was limited because the patient experienced recurrent aerophagia and subsequently underwent HGNS implantation. HGNS titration led to improved control of the patient’s OSA, but TE-CSA recurred and demonstrated a strong positional component. Lateral positional therapy was implemented with adequate control of respiratory events. TE-CSA can persist throughout different treatment modalities, including HGNS. The patient’s successful lateral sleep therapy for persistent and positionally exacerbated TE-CSA demonstrates the benefit of a well-known sleep apnea treatment for this poorly understood condition.
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Cohen, Scott, Paul Kileny, Ramon M. Esclamado, and Steven Telian. "Correlation between the Laryngeal Brain Stem Evoked Response and the Laryngeal Chemoreflex in the Porcine Model." Annals of Otology, Rhinology & Laryngology 102, no. 2 (February 1993): 92–99. http://dx.doi.org/10.1177/000348949310200203.
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The laryngeal brain stem evoked response (LBR) represents the neural activity involved in laryngeal reflex pathways. The laryngeal chemoreflex (LCR) is a centrally mediated response consisting of apnea and hemodynamic changes that result from laryngeal stimulation. The purpose of this study is to determine the characteristics of the LBR that are predictive of LCR severity in the porcine model. The duration of apnea resulting from stimulation of the supraglottic larynx defined LCR severity. The LBR tracings were recorded from electrodes flanking the brain stem following direct electrical stimulation of the superior laryngeal nerve. The LBR peak latencies from piglets demonstrating prolonged LCR apnea were compared to those without an exaggerated LCR response. Two LBR peak latencies demonstrated a statistically significant difference between the two piglet groups. These peak latencies appear to be indicators of susceptibility to exaggerated laryngeal reflex sensitivity. Thus, the LBR may prove useful in identifying and evaluating subjects predisposed to conditions associated with dysfunctional laryngeal reflex activity.