Journal articles on the topic 'Apnea'
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1
Baković, Darija, Zoran Valic, Davor Eterović, Ivica Vuković, Ante Obad, Ivana Marinović-Terzić, and Z̆eljko Dujić. "Spleen volume and blood flow response to repeated breath-hold apneas." Journal of Applied Physiology 95, no. 4 (October 2003): 1460–66. http://dx.doi.org/10.1152/japplphysiol.00221.2003.
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The purpose of this study was 1) to answer whether the reduction in spleen size in breath-hold apnea is an active contraction or a passive collapse secondary to reduced splenic arterial blood flow and 2) to monitor the spleen response to repeated breath-hold apneas. Ten trained apnea divers and 10 intact and 7 splenectomized untrained persons repeated five maximal apneas (A1-A5) with face immersion in cold water, with 2 min interposed between successive attempts. Ultrasonic monitoring of the spleen and noninvasive cardiopulmonary measurements were performed before, between apneas, and at times 0, 10, 20, 40, and 60 min after the last apnea. Blood flows in splenic artery and splenic vein were not significantly affected by breath-hold apnea. The duration of apneas peaked after A3 (143, 127, and 74 s in apnea divers, intact, and splenectomized persons, respectively). A rapid decrease in spleen volume (∼20% in both apnea divers and intact persons) was mainly completed throughout the first apnea. The spleen did not recover in size between apneas and only partly recovered 60 min after A5. The well-known physiological responses to apnea diving, i.e., bradycardia and increased blood pressure, were observed in A1 and remained unchanged throughout the following apneas. These results show rapid, probably active contraction of the spleen in response to breath-hold apnea in humans. Rapid spleen contraction and its slow recovery may contribute to prolongation of successive, briefly repeated apnea attempts.
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Chen, Ling, and Steven M. Scharf. "Systemic and myocardial hemodynamics during periodic obstructive apneas in sedated pigs." Journal of Applied Physiology 84, no. 4 (April 1, 1998): 1289–98. http://dx.doi.org/10.1152/jappl.1998.84.4.1289.
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The effects of periodic obstructive apneas on systemic and myocardial hemodynamics were studied in nine preinstrumented sedated pigs under four conditions: breathing room air (RA), breathing 100% O2, breathing RA after critical coronary stenosis (CS) of the left anterior descending coronary artery, and breathing RA after autonomic blockade with hexamethonium (Hex). Apneas with RA increased mean arterial pressure (MAP; from baseline 103.0 ± 3.5 to late apnea 123.6 ± 7.0 Torr, P < 0.001) and coronary blood flow (CBF; late apnea 193.9 ± 22.9% of baseline, P < 0.001) but decreased cardiac output (CO; from baseline 2.97 ± 0.15 to late apnea 2.39 ± 0.19 l/min, P < 0.001). Apneas with O2 increased MAP (from baseline 105.1 ± 4.6 to late apnea 110.7 ± 4.8 Torr, P < 0.001). Apneas with CS produced similar increases in MAP as apneas with RA but greater decreases in CO (from baseline 3.03 ± 0.19 to late apnea 2.1 ± 0.15 l/min, P < 0.001). In LAD-perfused myocardium, there was decreased segmental shortening (baseline 11.0 ± 1.5 to late apnea 7.6 ± 2.0%, P < 0.01) and regional intramyocardial pH (baseline 7.05 ± 0.03 to late apnea 6.72 ± 0.11, P < 0.001) during apneas with CS but under no other conditions. Apneas with Hex increased to the same extent as apneas with RA. Myocardial O2 demand remained unchanged during apnea relative to baseline. We conclude that obstructive apnea-induced changes in left ventricular afterload and CO are secondary to autonomic-mediated responses to hypoxemia. Increased CBF during apneas is related to regional metabolic effects of hypoxia and not to autonomic factors. In the presence of limited coronary flow reserve, decreased O2 supply during apneas can lead to myocardial ischemia, which in turn adversely affects left ventricular function.
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Basner, R. C., E. Onal, D. W. Carley, E. J. Stepanski, and M. Lopata. "Effect of induced transient arousal on obstructive apnea duration." Journal of Applied Physiology 78, no. 4 (April 1, 1995): 1469–76. http://dx.doi.org/10.1152/jappl.1995.78.4.1469.
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Six untreated male patients (age 19–55 yr) with obstructive sleep apnea underwent nocturnal polysomnography with acoustic stimulation to determine the effect of transient arousal on obstructive apneas during sleep. Binaural tone bursts (25–95 dB) were delivered in late expiration during the second obstructive apnea of a cycle consisting of four consecutive apneas. For the group, stimulated apneas were significantly shorter (P < 0.05, Fisher's protected least significant difference test) than were the unstimulated apneas when transient electrocortical arousal was elicited in both non-rapid-eye-movement (non-REM) sleep [mean 17 +/- 7 (SD) vs. 26 +/- 9, 23 +/- 10, and 26 +/- 12 s for 2nd vs. 1st, 3rd, and 4th apnea, respectively, of each cycle] and REM sleep (mean 19 +/- 10 vs. 35 +/- 15, 45 +/- 18, and 39 +/- 20 s). Without electrocortical arousal, the stimulated apnea was significantly shortened in non-REM (23 +/- 9 vs. 25 +/- 7, 24 +/- 8, and 26 +/- 8 s) but not in REM (32 +/- 16 vs. 37 +/- 12, 32 +/- 15, and 30 +/- 16 s). Tones delivered relatively early and late in the apnea were equally likely to be associated with resolution of the apnea. The nadir of arterial oxygen saturation of hemoglobin was inversely proportional to apnea length, with higher saturation nadirs associated with the stimulated apneas. These data indicate that transient arousal, induced by nonrespiratory stimulation, influences the resolution of obstructive apneas during sleep.
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Khan, Muhammad Talha, and Rose Amy Franco. "Complex Sleep Apnea Syndrome." Sleep Disorders 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/798487.
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Complex sleep apnea is the term used to describe a form of sleep disordered breathing in which repeated central apneas (>5/hour) persist or emerge when obstructive events are extinguished with positive airway pressure (PAP) and for which there is not a clear cause for the central apneas such as narcotics or systolic heart failure. The driving forces in the pathophysiology are felt to be ventilator instability associated oscillation in PaCO2arterial partial pressure of Carbon Dioxide, continuous cositive airway pressure (CPAP) related increased CO2carbon dioxide elimination, and activation of airway and pulmonary stretch receptors triggering these central apneas. The prevalence ranges from 0.56% to 18% with no clear predictive characteristics as compared to simple obstructive sleep apnea. Prognosis is similar to obstructive sleep apnea. The central apnea component in most patients on followup using CPAP therap, has resolved. For those with continued central apneas on simple CPAP therapy, other treatment options include bilevel PAP, adaptive servoventilation, permissive flow limitation and/or drugs.
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Badr, M. S., F. Toiber, J. B. Skatrud, and J. Dempsey. "Pharyngeal narrowing/occlusion during central sleep apnea." Journal of Applied Physiology 78, no. 5 (May 1, 1995): 1806–15. http://dx.doi.org/10.1152/jappl.1995.78.5.1806.
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We hypothesized that subatmospheric intraluminal pressure is not required for pharyngeal occlusion during sleep. Six normal subjects and six subjects with sleep apnea or hypopnea (SAH) were studied during non-rapid-eye-movement sleep. Pharyngeal patency was determined by using fiber-optic nasopharyngoscopy during spontaneous central sleep apnea (n = 4) and induced hypocapnic central apnea via nasal mechanical ventilation (n = 10). Complete pharyngeal occlusion occurred in 146 of 160 spontaneously occurring central apneas in patients with central sleep apnea syndrome. During induced hypocapnic central apnea, gradual progressive pharyngeal narrowing occurred. More pronounced narrowing was noted at the velopharynx relative to the oropharynx and in subjects with SAH relative to normals. Complete pharyngeal occlusion frequently occurred in subjects with SAH (31 of 44 apneas) but rarely occurred in normals (3 of 25 apneas). Resumption of inspiratory effort was associated with persistent narrowing or complete occlusion unless electroencephalogram signs of arousal were noted. Thus pharyngeal cross-sectional area is reduced during central apnea in the absence of inspiratory effort. Velopharyngeal narrowing consistently occurs during induced hypocapnic central apnea even in normal subjects. Complete pharyngeal occlusion occurs during spontaneous or induced central apnea in patients with SAH. We conclude that subatmospheric intraluminal pressure is not required for pharyngeal occlusion to occur. Pharyngeal narrowing or occlusion during central apnea may be due to passive collapse or active constriction.
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Anne, Pratibha, Rupa Koothirezhi, Ugorji Okorie, Minh Tam Ho, Brittany Monceaux, Cesar Liendo, Sheila Asghar, and Oleg Chernyshev. "833 Evolution of sleep disordered breathing types in heart failure." Sleep 44, Supplement_2 (May 1, 2021): A324—A325. http://dx.doi.org/10.1093/sleep/zsab072.830.
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Abstract Introduction Central sleep apnea is commonly seen in patients with heart failure. Here we present a case demonstrating shifting of predominant apneic events from central to obstructive type after placement of left ventricular assist device (LVAD) in end stage heart failure patient. Report of case(s) Case Presentation: 66 year-old African American male has past medical history of chronic congestive heart failure diabetes, hypertension, paroxysmal atrial fibrillation, anemia, hypothyroidism, chronic kidney disease and sleep apnea. Prior to his LVAD placement, his left ventricular ejection fraction (EF) was <10%. Patient was diagnosed with central sleep apnea with AHI of 58 (with 92% of apneic events being central events), oxygen nadir of 74%. Subsequently, patient had LVAD placed for symptomatic heart failure and repeat polysomnogram repeated at six month demonstrated an improved AHI of 45.8 with predominantly obstructive and mixed apneic events, with only 12.5% being central events. Conclusion This case report highlights not only the improvement of the sleep apnea in CHF treated with LVAD but also shows the shift of apneic events from predominantly central to obstructive type post LVAD. Support (if any) 1. Henein MY, Westaby S, Poole-Wilson PA, Cowie MR, Simonds AK. Resolution of central sleep apnoea following implantation of a left ventricular assist device. Int J Cardiol. 2010 Feb 4;138(3):317–9. PMID: 18752859. 2. Köhnlein T, Welte T, Tan LB, Elliott MW. Central sleep apnoea syndrome in patients with chronic heart disease: a critical review of the current literature. Thorax. 2002 Jun;57(6):547–54. PMID: 12037232 3. Monda C, Scala O, Paolillo S, Savarese G, Cecere M, D’Amore C, Parente A, Musella F, Mosca S, Filardi PP. Apnee notturne e scompenso cardiaco: fisiopatologia, diagnosi e terapia [Sleep apnea and heart failure: pathophysiology, diagnosis and therapy]. G Ital Cardiol (Rome). 2010 Nov;11(11):815–22. Italian. PMID: 21348318.
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Dueñas, E., G. Pinzón, LM Morón Duarte, MS Medina, and A. García. "Alteraciones respiratorias durante el sueño e hipertensión pulmonar en niños con síndrome de Down a 2.640 metros de altura." Iatreia 27, no. 4-S (January 11, 2015): S2. http://dx.doi.org/10.17533/udea.iatreia.21358.
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INTRODUCCIÓN El síndrome de apnea-hipopnea de sueño (SAHS) está presente en 2% a 3% de la población pediátrica general con una frecuencia más alta en niños con trastornos genéticos. La prevalencia del SAHS en el síndrome de Down (SD) es mayor del 30%. Hay informes de mayor prevalencia de alteraciones respiratorias durante el sueño (ARS) a gran altura, especialmente durante el ascenso rápido. No hay estudios acerca de la frecuencia y características de las ARS y del SAHS en niños con SD que viven a gran altura.OBJETIVO Describir la frecuencia y características de las ARS, la frecuencia de hipertensión pulmonar (HTP) y el comportamiento de la saturación de oxígeno (SpO2) en la vigilia, el sueño y durante eventos en niños con SD en Bogotá, una ciudad situada a gran altura sobre el nivel del mar (2.640 m), de acuerdo con la edad y el índice de masa corporal (IMC). MÉTODOS Estudio descriptivo transversal. Se incluyeron todos los niños con SD con sospecha de ARS remitidos para polisomnograma (PSG) a la Fundación Neumológica Colombiana entre octubre del 2011 y enero del 2013. Se definieron tres grupos: apnea obstructiva, apnea obstructiva y central y sin apneas.RESULTADOS Se incluyeron 74 niños, 36,5% de ellos de sexo femenino, con edad media de 4 años. El 47,3% presentó apnea obstructiva, más frecuente en los mayores de 2 años; 35,1% apnea obstructiva y central, más frecuente en los menores de 2 años, y 17,6 % no presentó apneas. Saturación de oxígeno (SpO2) promedio en apnea obstructiva: 84,6%; en apnea obstructiva y central: 81,8% y en los sin apnea: 86,9% (p = 0,058); 23% presentaron obesidad, 16% con apnea obstructiva. 53 pacientes tuvieron ecocardiograma: 28% con HTP, 53,3% tuvieron apnea obstructiva y 26,7% apnea obstructiva y central, no hubo diferencias significativas. SpO2 promedio en pacientes con HTP: 88,3% durante la vigilia, 86,2% durante el sueño REM, 85,7% durante el sueño no REM, sin diferencia significativa comparada con la de pacientes sin HTP.CONCLUSIONES La desaturación está presente en los niños con SD independientemente del tipo de apnea. Los menores de 2 años presentan con mayor frecuencia apneas centrales asociadas a las apneas obstructivas. La obesidad en pacientes con SD no es un factor determinante de la presencia de apneas e HTP. No hubo diferencia estadísticamente significativa entre el grupo con HTP en cuanto a la frecuencia de apneas y el nivel de saturación de oxígeno en comparación con el grupo sin HTP.
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Richardson, Matt, Robert de Bruijn, H. C. Holmberg, Glenn Björklund, Helena Haughey, and Erika Schagatay. "Increase of Hemoglobin Concentration After Maximal Apneas in Divers, Skiers, and Untrained Humans." Canadian Journal of Applied Physiology 30, no. 3 (June 1, 2005): 276–81. http://dx.doi.org/10.1139/h05-120.
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Human splenic contraction occurs both during apnea and maximal exercise, increasing the circulating erythrocyte volume. We investigated the hematological responses to 3 maximal apneas performed by elite apneic divers, elite cross-country skiers, and untrained subjects. Post-apnea hemoglobin concentration had increased in all groups, but especially in divers. The increases disappeared within 10 min of recovery. Apneic duration across apneas also increased the most in divers. Responses in divers could be more pronounced as a result of apnea training. Key words: breath hold, serial apneas, spleen contraction, cross-country skiing
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Peng, Ying-Jie, Xiuli Zhang, Anna Gridina, Irina Chupikova, David L. McCormick, Robert J. Thomas, Thomas E. Scammell, et al. "Complementary roles of gasotransmitters CO and H2S in sleep apnea." Proceedings of the National Academy of Sciences 114, no. 6 (January 23, 2017): 1413–18. http://dx.doi.org/10.1073/pnas.1620717114.
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Sleep apnea, which is the periodic cessation of breathing during sleep, is a major health problem affecting over 10 million people in the United States and is associated with several sequelae, including hypertension and stroke. Clinical studies suggest that abnormal carotid body (CB) activity may be a driver of sleep apnea. Because gaseous molecules are important determinants of CB activity, aberrations in their signaling could lead to sleep apnea. Here, we report that mice deficient in heme oxygenase-2 (HO-2), which generates the gaseous molecule carbon monoxide (CO), exhibit sleep apnea characterized by high apnea and hypopnea indices during rapid eye movement (REM) sleep. Similar high apnea and hypopnea indices were also noted in prehypertensive spontaneously hypertensive (SH) rats, which are known to exhibit CB hyperactivity. We identified the gaseous molecule hydrogen sulfide (H2S) as the major effector molecule driving apneas. Genetic ablation of the H2S-synthesizing enzyme cystathionine-γ-lyase (CSE) normalized breathing inHO-2−/−mice. Pharmacologic inhibition of CSE withl-propargyl glycine prevented apneas in bothHO-2−/−mice and SH rats. These observations demonstrate that dysregulated CO and H2S signaling in the CB leads to apneas and suggest that CSE inhibition may be a useful therapeutic intervention for preventing CB-driven sleep apnea.
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Ringler, J., R. C. Basner, R. Shannon, R. Schwartzstein, H. Manning, S. E. Weinberger, and J. W. Weiss. "Hypoxemia alone does not explain blood pressure elevations after obstructive apneas." Journal of Applied Physiology 69, no. 6 (December 1, 1990): 2143–48. http://dx.doi.org/10.1152/jappl.1990.69.6.2143.
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In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (SaO2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (SaO2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (SaO2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (SaO2 nadir 79-82%): 18.8 +/- 7.1 vs. 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P less than 0.01); and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.
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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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Suto, Y., and Y. Inoue. "Sleep Apnea Syndrome." Acta Radiologica 37, no. 1P1 (January 1996): 315–20. http://dx.doi.org/10.1177/02841851960371p166.
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Purpose: We attempted to determine the usefulness of high-speed MR imaging for evaluating the severity of sleep apnea syndrome (SAS) by comparing findings of pharyngeal obstruction obtained with high-speed MR with those of all-night polysomnography (PSG). Subjects and Methods: A total of 33 patients with SAS underwent turbo-FLASH MR examination, while awake and after i.v. injection of hydroxyzine hydrochloride. Serial images were examined by cinemode. Pharyngeal findings on MR were divided into single-site obstruction (SO) at the velopharynx, multiple-site obstruction (MO), and no obstruction (NO). PSG findings were analyzed to determine the predominant type of apnea, severity as evaluated by an apnea index (AI), and the lowest SaO2 value during sleep. Results: Seventy-five percent of the central apnea group had SO, and 70% of the mixed apneas had MO, while only 15% of the obstructed apneas had MO. The percentage of patients with severe SAS (AI of 20% or higher) was 48% for the SO, and 70% for the MO. The lowest SaO2 value tended to be low in the mixed apnea in the case of PSG, and tended to be low in the MO at MR examination. Conclusion: Analysis of pharyngeal dynamics using high-speed MR may provide some useful information for evaluating the severity of SAS.
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Slamowitz, D., L. Chen, and S. M. Scharf. "Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs." Journal of Applied Physiology 86, no. 6 (June 1, 1999): 1890–96. http://dx.doi.org/10.1152/jappl.1999.86.6.1890.
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There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 ± 25%, P < 0.05), systemic vascular resistance (SVR; +33 ± 16%, P < 0.0005), and heart rate (HR; +5 ± 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; −16 ± 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater (∼14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes.
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Orlowski, James P. "Cerebrospinal Fluid Endorphins and the Infant Apnea Syndrome." Pediatrics 78, no. 2 (August 1, 1986): 233–37. http://dx.doi.org/10.1542/peds.78.2.233.
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Cerebrospinal fluid (CSF) β-endorphin levels were determined in 16 patients with infant apnea syndrome and 34 control patients. A statistically significant difference (P ≤ .0001) was found with the infant apnea syndrome patients having β-endorphin levels of 14.7 ± 1.2 pmol/L (mean ± SE) and the controls having levels of 6.9 ± 0.6 pmol/L (mean ± SE). To test whether these elevated CSF β-endorphin levels were the result or the possible cause of the apneas, three patients with infant apnea syndrome and abnormal CSF β-endorphin levels participated in a study to determine whether a continuous low-dose infusion (10 ug/kg/h) of the narcotic antagonist naloxone would reduce the occurrence of apneas and respiratory pauses during all-night polysomnogram recordings. A fourth patient with documented apneas but normal CSF β-endorphin levels was also studied while on a regimen of naloxone. In the patients with infant apnea syndrome and abnormal CSF (β-endorphin levels, a significant (P ≤ .05) reduction in apneas and respiratory pauses occurred during naloxone infusion. There was no change in the occurrence of apneas or respiratory pauses during naloxone infusion in the patient with normal CSF endorphin levels. Abnormal CSF levels of endorphins may play a role in apneas of infancy and may be amenable to therapy with narcotic antagonists.
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Davis, Eric M., Landon W. Locke, Angela L. McDowell, Patrick J. Strollo, and Christopher P. O'Donnell. "Obesity accentuates circadian variability in breathing during sleep in mice but does not predispose to apnea." Journal of Applied Physiology 115, no. 4 (August 15, 2013): 474–82. http://dx.doi.org/10.1152/japplphysiol.00330.2013.
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Obesity is a primary risk factor for the development of obstructive sleep apnea in humans, but the impact of obesity on central sleep apnea is less clear. Given the comorbidities associated with obesity in humans, we developed techniques for long-term recording of diaphragmatic EMG activity and polysomnography in obese mice to assess breathing patterns during sleep and to determine the effect of obesity on apnea generation. We hypothesized that genetically obese ob/ob mice would exhibit less variability in breathing across the 24-h circadian cycle, be more prone to central apneas, and be more likely to exhibit patterns of increased diaphragm muscle activity consistent with obstructive apneas compared with lean mice. Unexpectedly, we found that obese mice exhibited a greater circadian impact on respiratory rate and diaphragmatic burst amplitude than lean mice, particularly during rapid eye movement (REM) sleep. Central apneas were more common in REM sleep (42 ± 17 h−1) than non-REM (NREM) sleep (14 ± 5 h−1) in obese mice ( P < 0.05), but rates were not different between lean and obese mice in either sleep state. Even after experimentally enhancing central apnea generation by acute withdrawal of hypoxic chemoreceptor activation during sleep, central apnea rates remained comparable between lean and obese mice. Last, we were unable to detect patterns of diaphragmatic burst activity suggestive of obstructive apnea events in obese mice. In summary, obesity does not predispose mice to increased occurrence of central or obstructive apneas during sleep, but does lead to a more pronounced circadian variability in respiration.
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Cala, S. J., P. Sliwinski, M. G. Cosio, and R. J. Kimoff. "Effect of topical upper airway anesthesia on apnea duration through the night in obstructive sleep apnea." Journal of Applied Physiology 81, no. 6 (December 1, 1996): 2618–26. http://dx.doi.org/10.1152/jappl.1996.81.6.2618.
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Cala, S. J., P. Sliwinski, M. G. Cosio, and R. J. Kimoff.Effect of topical upper airway anesthesia on apnea duration through the night in obstructive sleep apnea. J. Appl. Physiol. 81(6): 2618–2626, 1996.—It has previously been reported that the duration of obstructive apneas increases from the beginning to the end of the night (M. Charbonneau, J. M. Marin, A. Olha, R. J. Kimoff, R. D. Levy, and M. Cosio. Chest 106: 1695–1701, 1994). The purpose of this study was to test the hypothesis that stimulation of upper airway (UA) sensory receptors during obstructed inspiratory efforts contributes to arousal and apnea termination and that a progressive attenuation of this mechanism through the night contributes to apnea lengthening. We studied seven patients (six men, one woman) with severe obstructive sleep apnea (apnea-hypopnea index = 93 ± 26 events/h) during two consecutive nights of polysomnographic monitoring. On one night (random order), we performed topical UA anesthesia with 0.2% tetracaine and on the control night, sham anesthesia. We measured apnea duration, esophageal pressure (Pes) during apneas, and apneic O2 desaturation. Consistent with previous findings, apnea duration, number of efforts per apnea, and peak Pes at end apnea increased from the beginning to the end of the control nights. UA anesthesia produced a significant increase in apnea duration at the beginning of the night but no change in apnea length at the end of the night. Peak Pes and the rate of increase in Pes during the anesthesia nights were greater than during control nights, but the rate of increase in Pes was similar for the beginning and end of the control and anesthesia nights. These findings suggest that UA sensory receptors play a role in mediating apnea termination at the beginning of the night but that the contribution of these receptors diminishes as the night progresses such that greater inspiratory efforts are required to trigger arousal, leading to apnea prolongation.
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Yıldız, M. "The acute effects of repeated static apnea on aerobic power." Physical education of students 22, no. 4 (August 28, 2018): 217–20. http://dx.doi.org/10.15561/20755279.2018.0407.
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Purpose: Apnea exercises cause a rise in hematocrit, erythropoietin, hemoglobin concentration, lung volume and oxygen store in muscle and blood, and a decrease in blood acidosis and oxidative stress. These types of physiological changes that occur in the body result in developments in both time to exhaustion and V02max. The purpose of the current study was to investigate the acute effect of repeated static apneas on aerobic power. Material: Twenty physically active male university students (age:22.80±3.84 year, height:177.40±7.49 cm and weight:68.20±8.72 kg) volunteered to participate in the current study. They were divided as the static apnea and control groups randomly. The static group performed multistage exercise treadmill test to exhaustion (maximal aerobic power) after three maximal apneas with 2-min interval in sitting position. The control group performed only the maximal aerobic power test without apnea. Their maximal oxygen consumption (Vo2max), gas exchange rate (RER), heart beat rate (HR) and rate of perceived exertion (RPE) values were measured during maximal aerobic test. Their hemoglobin (Hb) and hematocrit (Hct) values were measured before and immediately after the apnea for both groups. Results: There were no significant differences found between the control and static apnea groups for Vo2max, HR, Hb and Hct. However, RPE values measured after the static apnea were lower (17.55±0.51) than the control (18.75±0.62). Conclusions: The repeated static apneas immediately prior the maximal aerobic effort cannot increase aerobic power in untrained breath hold participants. However, the lower RPE after static apnea may be used as an ergogenic effect.
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Cutler, Michael J., Nicolette Muenter Swift, David M. Keller, Wendy L. Wasmund, John R. Burk, and Michael L. Smith. "Periods of intermittent hypoxic apnea can alter chemoreflex control of sympathetic nerve activity in humans." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 5 (November 2004): H2054—H2060. http://dx.doi.org/10.1152/ajpheart.00377.2004.
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Obstructive sleep apnea is associated with sustained elevation of muscle sympathetic nerve activity (MSNA) and altered chemoreflex control of MSNA, both of which likely play an important role in the development of hypertension in these patients. Additionally, short-term exposure to intermittent hypoxic apneas can produce a sustained elevation of MSNA. Therefore, we tested the hypothesis that 20 min of intermittent hypoxic apneas can alter chemoreflex control of MSNA. Twenty-one subjects were randomly assigned to one of three groups (hypoxic apnea, hypercapnic hypoxia, and isocapnic hypoxia). Subjects were exposed to 30 s of the perturbation every minute for 20 min. Chemoreflex control of MSNA was assessed during baseline, 1 min posttreatment, and every 15 min throughout 180 min of recovery by the MSNA response to a single hypoxic apnea. Recovery hypoxic apneas were matched to a baseline hypoxic apnea with a similar nadir oxygen saturation. A significant main effect for chemoreflex control of MSNA was observed after 20 min of intermittent hypoxic apneas ( P < 0.001). The MSNA response to a single hypoxic apnea was attenuated 1 min postexposure compared with baseline ( P < 0.001), became augmented within 30 min of recovery, and remained augmented through 165 min of recovery ( P < 0.05). Comparison of treatment groups revealed no differences in the chemoreflex control of MSNA during recovery ( P = 0.69). These data support the hypothesis that 20 min of intermittent hypoxic apneas can alter chemoreflex control of MSNA. Furthermore, this response appears to be mediated by hypoxia.
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Waggener, T. B., I. D. Frantz, B. A. Cohlan, and A. R. Stark. "Mixed and obstructive apneas are related to ventilatory oscillations in premature infants." Journal of Applied Physiology 66, no. 6 (June 1, 1989): 2818–26. http://dx.doi.org/10.1152/jappl.1989.66.6.2818.
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In our previous study of 14 premature infants, apnea occurred at the minimum phase of ventilatory oscillations. The apneas corresponded to cessation of airflow at the nose and mouth and were not distinguished as central, mixed, or obstructive. Changes in heart rate associated with the apneas were not identified. To determine whether ventilatory pattern characteristics might predict either the type of apnea or heart rate changes during the apnea, we analyzed measurements of chest wall movement and heart rate that were made during the earlier studies. Chest wall movement measured by magnetometers was compared with airflow measured with a face mask and pneumotachograph. Tidal volume, breath duration, and ventilation were calculated on a breath-by-breath basis, converted to time-axis data strings, and filtered with a comb of zero phase shift digital band-pass filters to detect breathing patterns. Of 182 apneas greater than or equal to 3 s duration, 55% were central, 31% were mixed, and 14% were obstructive. All three types of apnea were related to ventilatory oscillations. Multiple linear and logistic regressions showed that an apnea was more likely to be obstructive when it was long and when the underlying ventilatory oscillation was due primarily to an oscillation in breath duration. Multiple linear and logistic regressions showed that decreases in heart rate were related primarily to the duration of apnea and secondarily to the characteristics of the underlying breathing patterns.
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Vaartjes, Martin, Rob L. M. Strijers, and Nico de Vries. "Posterior Nasal Packing and Sleep Apnea." American Journal of Rhinology 6, no. 2 (March 1992): 71–74. http://dx.doi.org/10.2500/105065892781874784.
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Posterior nasal packing has been reported to be associated with cardiorespiratory complications and, occasionally, with sudden death. To study the rate and incidence of sleep apnea, between October 1989 and September 1990 polysomnography (PSG) was performed in 10 patients who were treated for severe epistaxis with posterior nasal packing. Of these 10 patients, three had obstructive apneas, one had central apneas, and four had a combination of central and/or obstructive and mixed apneas. One patient had no apneas, and one was unable to sleep during PSG. In six patients, PSG was repeated a few months after removal of the packs. Four of these six patients no longer had apneas; one patient had a considerable decrease in number of apneas. One patient did not sleep during the second PSG, however, he had no apneas during the first PSG. This study demonstrates that posterior nasal packing can induce sleep apneas or enhance the severity of an apnea syndrome when present. This may contribute to the cardiorespiratory morbidity and sudden death that has been reported in epistaxis patients treated with posterior packing.
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Schneider, H., C. D. Schaub, C. A. Chen, K. A. Andreoni, A. R. Schwartz, P. L. Smith, J. L. Robotham, and C. P. O'Donnell. "Effects of arousal and sleep state on systemic and pulmonary hemodynamics in obstructive apnea." Journal of Applied Physiology 88, no. 3 (March 1, 2000): 1084–92. http://dx.doi.org/10.1152/jappl.2000.88.3.1084.
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During obstructive sleep apnea (OSA), systemic (Psa) and pulmonary (Ppa) arterial pressures acutely increase after apnea termination, whereas left and right ventricular stroke volumes (SV) reach a nadir. In a canine model ( n = 6), we examined the effects of arousal, parasympathetic blockade (atropine 1 mg/kg iv), and sleep state on cardiovascular responses to OSA. In the absence of arousal, SV remained constant after apnea termination, compared with a 4.4 ± 1.7% decrease after apnea with arousal ( P < 0.025). The rise in transmural Ppa was independent of arousal (4.5 ± 1.0 vs. 4.1 ± 1.2 mmHg with and without arousal, respectively), whereas Psa increased more after apnea termination in apneas with arousal compared with apneas without arousal. Parasympathetic blockade abolished the arousal-induced increase in Psa, indicating that arousal is associated with a vagal withdrawal of the parasympathetic tone to the heart. Rapid-eye-movement (REM) sleep blunted the increase in Psa (pre- to end-apnea: 5.6 ± 2.3 mmHg vs. 10.3 ± 1.6 mmHg, REM vs. non-REM, respectively, P< 0.025), but not transmural Ppa, during an obstructive apnea. We conclude that arousal and sleep state both have differential effects on the systemic and pulmonary circulation in OSA, indicating that, in patients with underlying cardiovascular disease, the hemodynamic consequences of OSA may be different for the right or the left side of the circulation.
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Dempsey, Jerome A. "Central sleep apnea: misunderstood and mistreated!" F1000Research 8 (June 28, 2019): 981. http://dx.doi.org/10.12688/f1000research.18358.1.
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Central sleep apnea is prevalent in patients with heart failure, healthy individuals at high altitudes, and chronic opiate users and in the initiation of “mixed” (that is, central plus obstructive apneas). This brief review focuses on (a) the causes of repetitive, cyclical central apneas as mediated primarily through enhanced sensitivities in the respiratory control system and (b) treatment of central sleep apnea through modification of key components of neurochemical control as opposed to the current universal use of positive airway pressure.
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Henke, K. G., and C. E. Sullivan. "Effects of high-frequency pressure waves applied to upper airway on respiration in central apnea." Journal of Applied Physiology 73, no. 3 (September 1, 1992): 1141–45. http://dx.doi.org/10.1152/jappl.1992.73.3.1141.
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We examined the effects of high-frequency (30-Hz) low-pressure oscillations on respiration in nine patients with central sleep apnea. All patients were studied during sleep and wore a nasal mask through which the oscillations were applied. All tests were performed during periods of repetitive central apneas. Respiratory efforts were monitored from the airflow and calibrated Respitrace signals. After several cycles of apnea were monitored, the oscillatory pressures were applied for brief periods (less than 5 s) at the midpoint of the central apneas. All trials in which arousal occurred were discarded, leaving a total of 106 trials in the nine patients. High-frequency oscillation of the upper airway stimulated respiratory effort(s) in 68% of all trials (72 of 106). Apnea length was significantly shortened in four of the nine patients. In one patient with a tracheostomy, the stimulus applied to his isolated upper airway evoked respiratory efforts during central apnea in 13 of 15 trials. We conclude that high-frequency oscillatory pressures applied to the upper airway can stimulate respiratory efforts during central apnea. This response may be mediated by upper airway receptors involved in nonrespiratory airway defense reflexes and may have implications in the treatment of patients with central sleep apnea.
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Insalaco, G., S. T. Kuna, G. Catania, O. Marrone, B. M. Costanza, V. Bellia, and G. Bonsignore. "Thyroarytenoid muscle activity in sleep apneas." Journal of Applied Physiology 74, no. 2 (February 1, 1993): 704–9. http://dx.doi.org/10.1152/jappl.1993.74.2.704.
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In normal subjects the thyroarytenoid muscle (TA), a vocal cord adductor, has phasic expiratory activity during wakefulness that disappears during non-rapid-eye-movement (NREM) sleep. Fiber-optic studies have reported absent or irregular vocal cord movements during obstructive apneas and vocal cord adduction during central apneas. This study was designed to investigate TA activity during NREM sleep in 14 subjects with sleep apnea by means of intramuscular wire electrodes. During central apneas, which were recorded in three subjects, continuous TA activity was observed. During obstructive apneas, which were recorded in all subjects, two different patterns of TA activity were observed: 1) absence of any activity until arousal and 2) phasic activity throughout the apnea. The first pattern was detected in six subjects, whereas both patterns were observed in the remaining eight subjects. No correlation was found between obstructive apnea characteristics and presence or absence of TA activity. In all subjects TA underwent a marked activation during arousal. While nasal continuous positive airway pressure was applied during NREM sleep TA activity was always absent. The persistence of TA activity during central apneas suggests that they may represent an extreme prolongation of neural expiratory discharge. We speculate that a variable interaction of different stimuli acting during obstructive apnea may activate TA, which, in turn, may contribute to glottic narrowing.
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Nakamura, Akira, Yasuichiro Fukuda, and Tomoyuki Kuwaki. "Sleep apnea and effect of chemostimulation on breathing instability in mice." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 525–32. http://dx.doi.org/10.1152/japplphysiol.00226.2002.
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Sleep apnea occurs in humans and experimental animals. We examined whether it also arises in adult mice. Ventilation in male adult 129/Sv mice was recorded concomitantly by electroencephalograms and electromyograms for 6 h by use of body plethysmography. Apnea was defined as cessation of plethysmographic signals for longer than two respiratory cycles. While mice breathed room air, 32.3 ± 6.9 (mean ± SE, n = 5) apneas were observed during sleep but not in quiet awake periods. Sleep apneas were further classified into two types. Postsigh apneas occurred exclusively during slow-wave sleep (SWS), whereas spontaneous apneas arose during both SWS and rapid eye movement sleep. Compared with room air (9.1 ± 1.4/h of SWS), postsigh apneas were more frequent in hypoxia (13.7 ± 2.1) and less frequent in hyperoxia (3.6 ± 1.7) and hypercapnia (2.8 ± 2.1). Our data indicated that significant sleep apnea occurs in normal adult mice and suggested that the mouse could be a promising experimental model with which to study the genetic and molecular basis of respiratory regulation during sleep.
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Fletcher, E. C., S. Goodnight, T. Miller, R. A. Luckett, J. Rosborough, D. Munafo, and S. Muniz. "Atelectasis affects the rate of arterial desaturation during obstructive apnea." Journal of Applied Physiology 69, no. 5 (November 1, 1990): 1863–68. http://dx.doi.org/10.1152/jappl.1990.69.5.1863.
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Chronic hemodynamic disturbances are more profound in patients with obstructive sleep apnea when underlying lung disease with abnormal gas exchange (low arterial PO2) is present. Previous studies suggest that pulmonary gas exchange could influence the rate of fall of arterial oxygen saturation (dSaO2/dt) in obstructive sleep apnea. We postulated that abnormal gas exchange in the form of atelectasis would steepen dSaO2/dt and thereby lower nadir arterial oxyhemoglobin saturation (SaO2) for the same duration of apnea. Apneas were created by clamping an indwelling cuffed endotracheal tube at end expiration in eight spontaneously breathing adult baboons. Apneas of the same duration were then repeated during temporary endobronchial occlusion of one lobe of the lung. SaO2 and mixed venous O2 saturation were continuously monitored, and cardiac output was calculated. Worsening of pulmonary gas exchange during atelectasis was documented by an increase in calculated venous admixture from 10.5 +/- 0.8 to 25.0 +/- 0.7% (P less than 0.001). The dSaO2/dt was independent of apnea duration at 30, 45, and 60 s. During endobronchial occlusion, apnea dSaO2/dt increased 20%, and nadir SaO2 was significantly lower. Possible mechanisms for steepening of dSaO2/dt during atelectasis are discussed.
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Bezruk, Dmitriy, Petr Bahenský, David Marko, Miroslav Krajcigr, Petr Bahenský, Eva Novák-Nowická, and Tomáš Mrkvička. "The Effect of Static Apnea Diving Training on the Physiological Parameters of People with a Sports Orientation and Sedentary Participants: A Pilot Study." Sports 12, no. 6 (May 22, 2024): 140. http://dx.doi.org/10.3390/sports12060140.
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Diver training improves physical and mental fitness, which can also benefit other sports. This study investigates the effect of eight weeks of static apnea training on maximum apnea time, and on the physiological parameters of runners, swimmers, and sedentary participants, such as forced vital capacity (FVC), minimum heart rate (HR), and oxygen saturation (SpO2). The study followed 19 participants, including five runners, swimmers, sedentary participants, and four competitive divers for reference values. The minimum value of SpO2, HR, maximum duration of apnea, and FVC were measured. Apnea training occurred four times weekly, consisting of six apneas with 60 s breathing pauses. Apnea duration was gradually increased by 30 s. The measurement started with a 30 s apnea and ended with maximal apnea. There was a change in SpO2 decreased by 6.8%, maximum apnea length increased by 15.8%, HR decreased by 9.1%, and FVC increased by 12.4% for the groups (p < 0.05). There were intra-groups changes, but no significant inter-groups difference was observed. Eight weeks of apnea training improved the maximum duration of apnea, FVC values and reduced the minimum values of SpO2 and HR in all groups. No differences were noted between groups after training. This training may benefit cardiorespiratory parameters in the population.
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Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley. "Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea." Journal of Applied Physiology 82, no. 3 (March 1, 1997): 918–26. http://dx.doi.org/10.1152/jappl.1997.82.3.918.
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Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley. Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea. J. Appl. Physiol. 82(3): 918–926, 1997.—We hypothesized that reductions in arterial [Formula: see text]([Formula: see text]) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising[Formula: see text] would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous[Formula: see text] were measured: during room air breathing ( N1), alternating room air and CO2 breathing ( N2), CO2 breathing all night ( N3), and addition of dead space via a face mask all night ( N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous [Formula: see text], which virtually eliminated apneas and hypopneas; they decreased from 43.7 ± 7.3 apneas and hypopneas/h on N1 to 5.8 ± 0.9 apneas and hypopneas/h during N3( P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 ( P< 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 ( P< 0.005). Because raising[Formula: see text] through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in[Formula: see text] below the apnea threshold.
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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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Fletcher, E. C., R. Kass, J. I. Thornby, J. Rosborough, and T. Miller. "Central venous O2 saturation and rate of arterial desaturation during obstructive apnea." Journal of Applied Physiology 66, no. 3 (March 1, 1989): 1477–85. http://dx.doi.org/10.1152/jappl.1989.66.3.1477.
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We examined the rate of fall of arterial O2 saturation (dSao2/dt) after apnea onset in four spontaneously breathing adult male baboons. We postulated that a lower mixed venous O2 saturation (Svo2) would steepen dSao2/dt by more rapid depletion of alveolar O2. Single isolated (NREP) and five or more sequential repetitive apneas (REP) were created by clamping an indwelling cuffed endotracheal tube at end expiration. Fiberoptic catheters were used for continuous monitoring of Sao2, Svo2, and cardiac output. The mean dSao2/dt for all duration NREP apneas was 0.60%/s. Mean dSao2/dt increased above base line for each consecutive REP apnea and was higher in 60 s than in 45 and 30 s REP apnea series. The increase in dSao2/dt corresponded closely with the fall in preapneic Svo2. Preapneic arterial O2 content fell during successive REP apneas but the maximal decrement from base line (1.3 ml/dl) was much less than the maximal decrement in preapneic mixed venous O2 content of 5.1 ml/dl. Preapneic cardiac output for NREP apneas and nadir cardiac output for REP apneas remained constant. Nadir cardiac output for NREP apneas showed higher values for longer duration apneas. We concluded that dSao2/dt is inversely related to preapneic Svo2.
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Fairbanks, David W., and David N. F. Fairbanks. "Neurostimulation for Obstructive Sleep Apnea: Investigations." Ear, Nose & Throat Journal 72, no. 1 (January 1993): 52–57. http://dx.doi.org/10.1177/014556139307200111.
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Neurostimulation of the upper airway muscles (accessory muscles of respiration) was accomplished in anesthetized dogs and sleeping humans by electrical stimulation of the hypoglossal nerves. Such stimulations relieved partial airway obstructions in dogs. They also aborted (shortened) obstructive sleep apnea events in humans who suffer with obstructive sleep apnea syndrome. In one subject, stimulations delivered in advance of apneic events (by automatic cycling) prevented apneas. Neurostimulation for obstructive sleep apnea may be an important concept for future research and development.
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Akbarian, Sina, Nasim Montazeri Ghahjaverestan, Azadeh Yadollahi, and Babak Taati. "Distinguishing Obstructive Versus Central Apneas in Infrared Video of Sleep Using Deep Learning: Validation Study." Journal of Medical Internet Research 22, no. 5 (May 22, 2020): e17252. http://dx.doi.org/10.2196/17252.
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Background Sleep apnea is a respiratory disorder characterized by an intermittent reduction (hypopnea) or cessation (apnea) of breathing during sleep. Depending on the presence of a breathing effort, sleep apnea is divided into obstructive sleep apnea (OSA) and central sleep apnea (CSA) based on the different pathologies involved. If the majority of apneas in a person are obstructive, they will be diagnosed as OSA or otherwise as CSA. In addition, as it is challenging and highly controversial to divide hypopneas into central or obstructive, the decision about sleep apnea type (OSA vs CSA) is made based on apneas only. Choosing the appropriate treatment relies on distinguishing between obstructive apnea (OA) and central apnea (CA). Objective The objective of this study was to develop a noncontact method to distinguish between OAs and CAs. Methods Five different computer vision-based algorithms were used to process infrared (IR) video data to track and analyze body movements to differentiate different types of apnea (OA vs CA). In the first two methods, supervised classifiers were trained to process optical flow information. In the remaining three methods, a convolutional neural network (CNN) was designed to extract distinctive features from optical flow and to distinguish OA from CA. Results Overnight sleeping data of 42 participants (mean age 53, SD 15 years; mean BMI 30, SD 7 kg/m2; 27 men and 15 women; mean number of OA 16, SD 30; mean number of CA 3, SD 7; mean apnea-hypopnea index 27, SD 31 events/hour; mean sleep duration 5 hours, SD 1 hour) were collected for this study. The test and train data were recorded in two separate laboratory rooms. The best-performing model (3D-CNN) obtained 95% accuracy and an F1 score of 89% in differentiating OA vs CA. Conclusions In this study, the first vision-based method was developed that differentiates apnea types (OA vs CA). The developed algorithm tracks and analyses chest and abdominal movements captured via an IR video camera. Unlike previously developed approaches, this method does not require any attachment to a user that could potentially alter the sleeping condition.
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Christon, J., D. W. Carley, D. Monti, and M. Radulovacki. "Effects of inspired gas on sleep-related apnea in the rat." Journal of Applied Physiology 80, no. 6 (June 1, 1996): 2102–7. http://dx.doi.org/10.1152/jappl.1996.80.6.2102.
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Central apneas have been reported to occur in the rat during all stages of sleep. Two types of apnea have been described: spontaneous and postsigh, which are immediately preceded by an augmented breath. We studied the effect of inspired gas on the number and type of apneas in nine adult male Sprague-Dawley rats that were surgically prepared with cortical electroencephalogram and nuchal electromyogram electrodes. In addition to the electroencephalogram and electromyogram, we recorded respiration by the barometric method by using a single-chamber plethysmograph. Each rat was recorded from 1000 until 1600 on 4 separate days by using different inspired gases: room air, 100% O2, 15% O2, and 5% CO2. We found that the sleep-related apnea index was significantly higher during 100% O2 compared with room air (P < 0.05) and was significantly lower during 15% O2 and 5% CO2 compared with room air (P < 0.05). Postsigh apneas occurred more frequently than did spontaneous apneas (P < 0.0001). The coupling between sighs and apneas was strengthened by hyperoxia and weakened by hypoxia and hypercapnia (P < 0.05 for each). We conclude that stimulation of chemoreceptors acts to oppose apnea in the rat.
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Don, Garrick W., and Karen A. Waters. "Influence of sleep state on frequency of swallowing, apnea, and arousal in human infants." Journal of Applied Physiology 94, no. 6 (June 1, 2003): 2456–64. http://dx.doi.org/10.1152/japplphysiol.00361.2002.
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Apnea and arousal are modulated with sleep stage, and swallowing may interfere with respiratory rhythm in infants. We hypothesized that swallowing itself would display interaction with sleep state. Concurrent polysomnography and measurement of swallowing allowed time-matched analysis of 3,092 swallows, 482 apneas, and 771 arousals in 17 infants aged 1–34 wk. The mean rates of swallowing, apnea, and arousal were significantly different, being 23.3 ± 8.5, 9.4 ± 8.8, and 15.5 ± 10.6 h−1, respectively ( P < 0.001 ANOVA). Swallows occurred before 25.2 ± 7.9% and during 74.8 ± 6.3% of apneas and before 39.8 ± 6.0% and during 60.2 ± 6.0% of arousals. The frequencies of apneas and arousals were both strongly influenced by sleep state (active sleep > indeterminate > quiet sleep, P < 0.001), whether or not the events coincided with swallowing, but swallowing rate showed minimal independent interaction with sleep state. Interactions between swallowing and sleep state were predominantly influenced by the coincidence of swallowing with apnea or arousal.
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Jain, Vivek, Joseph Marbach, Shawn Kimbro, David C. Andrade, Arad Jain, Eleanor Capozzi, Kyle Mele, Rodrigo Del Rio, Matthew W. Kay, and David Mendelowitz. "Benefits of oxytocin administration in obstructive sleep apnea." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 5 (November 1, 2017): L825—L833. http://dx.doi.org/10.1152/ajplung.00206.2017.
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Activation of oxytocin receptors has shown benefits in animal models of obstructive sleep apnea (OSA). We tested if nocturnal oxytocin administration could have beneficial effects in OSA patients. Eight patients diagnosed with OSA were administered intranasal oxytocin (40 IU). Changes in cardiorespiratory events during sleep, including apnea and hypopnea durations and frequency, risk of event-associated arousals, and heart rate variability, were assessed. Oxytocin significantly increased indexes of parasympathetic activity, including heart rate variability, total sleep time, and the postpolysommogram sleep assessment score, an index of self-reported sleep satisfaction. Although the apnea-hypopnea index was not significantly changed with oxytocin administration, when apnea and hypopnea events were compared independently, the frequency of hypopneas, but not apneas, was significantly ( P ≤ 0.005) decreased with oxytocin treatment. Both apneas and hypopneas were significantly shortened in duration with oxytocin treatment. Oxytocin treatment significantly decreased the percent of apnea and hypopnea events that were accompanied with an arousal. Oxytocin administration has the potential to restore cardiorespiratory homeostasis and reduce some clinically important (objective and patient-reported) adverse events that occur with OSA. Additional studies are needed to further understand the mechanisms by which oxytocin promotes these changes in cardiorespiratory and autonomic function in OSA patients.
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Alvaro, R., J. Alvarez, K. Kwiatkowski, D. Cates, and H. Rigatto. "Induction of mixed apneas by inhalation of 100% oxygen in preterm infants." Journal of Applied Physiology 77, no. 4 (October 1, 1994): 1666–70. http://dx.doi.org/10.1152/jappl.1994.77.4.1666.
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Administration of 100% O2 to preterm infants induces an apnea that is usually central. We hypothesized that this apnea may be “mixed” at times with an obstructive component appearing late during the respiratory pause. In addition, we reasoned that obstruction would depend on the duration of the apnea. Thus, we gave 100% O2 to 61 healthy preterm infants. Group 1 was > or = 1,500 g [birth wt 1.8 +/- 0.1 (SE) kg, gestational age 32 +/- 1 wk, postnatal age 19 +/- 2 days, n = 26] and group 2 was < 1,500 g [birth wt 1.2 +/- 0.1 kg, gestational age 29 +/- 1 wk, postnatal age 30 +/- 4 days, n = 35]. Ventilation was measured using a flow-through system. Respiratory efforts in the absence of flow were detected using chest and abdominal displacements or diaphragmatic electromyography. In group 1, 19% of the central apneas became obstructive at 17 +/- 3 s, whereas in group 2, 34% did so at 12 +/- 2 s. Mixed apneas were longer than those without obstruction (28 +/- 3 vs. 12 +/- 1 s; P = 0.0001). The incidence of mixed apneas was 0, 14, and 66% in group 1 and 0, 27, and 69% in group 2 in apneas of 3–10, 11–20, and > 20 s, respectively. These findings suggest that 1) a percentage of the central apneas induced by inhaling 100% O2 became obstructive, 2) the incidence of the obstructive component increased with the duration of apnea, and 3) smaller infants became obstructed sooner and had a higher incidence of obstruction than larger infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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Chen, Ling, and Steven M. Scharf. "Effects of aortic nerve on hemodynamic response to obstructive apnea in sedated pigs." Journal of Applied Physiology 89, no. 4 (October 1, 2000): 1455–61. http://dx.doi.org/10.1152/jappl.2000.89.4.1455.
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In this study we test the hypothesis that aortic nerve traffic is responsible for the pressor response to periodic apneas. In nine intubated, sedated chronically instrumented pigs, periodic obstructive apneas were caused by occlusion of the endotracheal tube for 30 s, followed by spontaneous breathing for 30 s. This was done under control (C) conditions, after section of the aortic nerve (ANS), and after bilateral cervical vagotomy (Vagot). Blood-gas tensions and airway pressure changed similarly under all conditions: Po 2 decreased to 50–60 Torr, Pco 2 increased to ∼55 Torr, and airway pressure decreased by 40–50 mmHg during apnea. With C, mean arterial pressure (MAP) increased from 111 ± 4 mmHg at baseline to 120 ± 5 mmHg at late apnea ( P < 0.01). After ANS and Vagot, there was no change in MAP with apneas compared with baseline. Relative to baseline, cardiac output and stroke volume decreased with C but not with ANS or Vagot during apneas. Increased MAP was due to increased systemic vascular resistance. Heart rate behaved similarly with C and ANS, being greater at early interapnea than late apnea. With Vagot, heart rate increased throughout the apnea-interapnea cycle relative to baseline. We conclude that, in sedated pigs, aortic nerve traffic mediates the increase in MAP and systemic vascular resistance observed during periodic apneas. Increase in MAP is responsible for decreased cardiac output and stroke volume. Additional vagal reflexes, most likely parasympathetic efferents, are responsible for interacting with sympathetic excitatory influences in modulating heart rate.
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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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Crossland, Randy F., David J. Durgan, Eric E. Lloyd, Sharon C. Phillips, Anilkumar K. Reddy, Sean P. Marrelli, and Robert M. Bryan. "A new rodent model for obstructive sleep apnea: effects on ATP-mediated dilations in cerebral arteries." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 4 (August 15, 2013): R334—R342. http://dx.doi.org/10.1152/ajpregu.00244.2013.
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Obstructive sleep apnea (OSA), a condition in which the upper airway collapses during sleep, is strongly associated with metabolic and cardiovascular diseases. Little is known how OSA affects the cerebral circulation. The goals of this study were 1) to develop a rat model of chronic OSA that involved apnea and 2) to test the hypothesis that 4 wk of apneas during the sleep cycle alters endothelium-mediated dilations in middle cerebral arteries (MCAs). An obstruction device, which was chronically implanted into the trachea of rats, inflated to obstruct the airway 30 times/h for 8 h during the sleep cycle. After 4 wk of apneas, MCAs were isolated, pressurized, and exposed to luminally applied ATP, an endothelial P2Y2 receptor agonist that dilates through endothelial-derived nitric oxide (NO) and endothelial-dependent hyperpolarization (EDH). Dilations to ATP were attenuated ∼30% in MCAs from rats undergoing apneas compared with those from a sham control group ( P < 0.04 group effect; n = 7 and 10, respectively). When the NO component of the dilation was blocked to isolate the EDH component, the response to ATP in MCAs from the sham and apnea groups was similar. This finding suggests that the attenuated dilation to ATP must occur through reduced NO. In summary, we have successfully developed a novel rat model for chronic OSA that incorporates apnea during the sleep cycle. Using this model, we demonstrate that endothelial dysfunction occurred by 4 wk of apnea, likely increasing the vulnerability of the brain to cerebrovascular related accidents.
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Rani, Seema, Alexandra Cohen, Abigail Strang, and Aaron Chidekel. "1220 Polysomnography in Children with Joubert Syndrome." SLEEP 47, Supplement_1 (April 20, 2024): A520. http://dx.doi.org/10.1093/sleep/zsae067.01220.
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Abstract Introduction Joubert syndrome is autosomal recessive, clinically and genetically heterogeneous with multiorgan involvement. Classic breathing symptoms include episodes of hyperpnea followed by apnea and periodic breathing. Gas exchange abnormalities include hyperventilation with low CO2s and intermittent desaturations. Purpose of this abstract is to report prolonged survival, describe the PSG findings and treatment modalities in 2 cases. Report of case(s) 8-year-old female with Joubert syndrome, global developmental delay, hydrocephalus, hypotonia, cortical blindness presented for initial evaluation of sleep apnea. PSG revealed primarily central sleep apnea with upper airway resistance with snoring with arousal and few episodes of obstructive and mixed apnea and hypopnea. Gas exchange demonstrated episodic, brief desaturations, associated with central apneas. Repeat PSG at 13 years showed intermittent hyperpnea followed by apnea, low ETCO2s with self-limiting desaturations and periodic breathing. Gas exchange revealed low ETCO2 and desaturations. She was treated with clinical observation. PSG at age 20 year demonstrated intermittent hyperpnea followed by episodes of prolonged central apneas, with low ETCO2s and desaturations, and few obstructive hypopneas. Most central apneas associated with self-limiting desaturations, with significant number associated with oxygen saturation below 90%. Gas exchange demonstrated low ETCO2s and episodic desaturations. Supplemental oxygen was prescribed. 20-month-old female with diagnosed Joubert syndrome, cleft lip, polydactyly, hypotonia, dysphagia, and developmental delay presented for loud snoring and gasping during sleep and apneas while awake. Sibling with Joubert Syndrome and a tracheostomy had died. Presented for a second opinion for tracheostomy due to PSG at OSH demonstrating OSAHS with AHI of 18.2, OAI of 3.9 and CAI of 14.3, minimal hypoxemia, normal ETCO2 and SaO2 nadir was 75%. Repeat sleep study done at our center; AHI of 27.7 and OAI of 0.83. ETCO2 was normal, SpO2 nadir was 75% and minimal hypoxemia. Overall PSG demonstrated primarily central apneas with a few obstructive apneas and hypopneas and minimal O2 desaturations. Subsequently underwent BLPAP titration study and treated with non-invasive modality. Conclusion PSG in Joubert syndrome demonstrated intermittent hyperpnea and prolonged central apneas with low ETCO2's and brief desaturations. All events were predominantly present in REM sleep. Patients did well with low respiratory support and did not require tracheostomy. Support (if any)
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Toubas, Paul L., James C. Duke, Mary Anne McCaffree, Cynthia D. Mattice, Debra Bendell, and William C. Orr. "Effects of Maternal Smoking and Caffeine Habits on Infantile Apnea: A Retrospective Study." Pediatrics 78, no. 1 (July 1, 1986): 159–63. http://dx.doi.org/10.1542/peds.78.1.159.
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To evaluate the relationship of antecedent maternal smoking and caffeine consumption habits on the occurrence of apnea in their offspring, rates for central and obstructive apnea were analyzed in a cohort of mother-infant pairs. The mothers of 298 infants with apnea responded to a questionnaire completed prior to a nine-hour polysomnogram performed as part of the patients' evaluations. Cigarette consumption estimates were computed on a 20-cigarette per pack basis, and caffeine intake, based on dietary sources (coffee, tea, chocolate, and colas), was summarized as milligrams of caffeine consumed per day. Rates of central and obstructive apnea of 6 to 10 seconds in duration were calculated. Multiple linear regression analysis determined that smokers tended to be younger and have lower birth weight infants who presented earlier with apnea than infants of nonsmokers. Increased rates of central apnea occurred in infants of smokers as compared with infants of nonsmokers. During pregnancy, a pack per day increase in maternal smoking habit was associated with a 1.88/h increase in central apneas in their offspring (P <.01). Maternal smoking after delivery had a similar relationship. Obstructive apnea rates were similar in both groups. Both central and obstructive apnea rates associated positively with increasing maternal caffeine consumption. Smoking habits and caffeine ingestion were correlated (P < .01). Infants with apnea have greater rates of central apnea when their mothers smoke during pregnancy. Therefore, a history of nicotine consumption should be included in the medical history of infants presenting with apnea.
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Colvert, Jared, and Glen Greenough. "825 Central Sleep Apnea and Sinus Bradycardia." Sleep 44, Supplement_2 (May 1, 2021): A322. http://dx.doi.org/10.1093/sleep/zsab072.822.
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Abstract Introduction Central sleep apnea (CSA) is characterized by a lack of respiratory drive during sleep resulting in repetitive periods of apneas. There are multiple manifestations of CSA as defined by the ICSD3. CSA with Cheyne-Stokes Breathing (CSB) is characterized by a series of crescendo-decrescendo pattern of ventilation followed by central apnea and is often associated with heart failure. Bradyarrythmias have been associated with obstructive sleep apnea (OSA), but an association with central sleep apnea is less clear. Report of case(s) A 76 y/o male with no significant past medical history but with multiple instances of sinus bradycardia on previous EKGs, was referred to sleep medicine for evaluation of snoring, witnessed apneas, and daytime sleepiness. He had no history of CVA, CHF, atrial fibrillation, renal disease, or opioid use. PSG was completed for suspected OSA, and revealed moderate CSA (AHI 10.9 using hypopnea type 1B criteria, CAI 6.1). Central apneas at the latter portion of the study were consistent with a CSA-CSB. Awake heart rate at time of study was 44 bpm. During sleep, his heart rate ranged from 39–89 with a mean of 57 bpm. Due to this unexpected central apnea finding, cardiac evaluation was recommended and echocardiogram revealed a LVEF of 51%, a dilated left atrium, normal left ventricle chamber size, no wall motion abnormalities, and an inability to assess left sided filling pressures. EKG was consistent with sinus bradycardia without AV blocks. Holter monitor revealed sinus rhythm with moderate burden of ectopy. He underwent CPAP titration which revealed an effective CPAP pressure to control obstructive events, but central apneas persisted without CSB pattern. Conclusion In this patient, CSA/CSA-CSB was found in the absence of known risk factors for CSA. Although potentially an early sign of HFpEF related to his longstanding sinus bradycardia, this case raises the question as to whether sinus bradycardia in isolation could decrease cardiac output enough to destabilize ventilation and promote this finding of CSA/CSA-CSB. Support (if any):
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Miller, M. J., T. G. Petrie, and J. M. Difiore. "Changes in resistance and ventilatory timing that accompany apnea in premature infants." Journal of Applied Physiology 75, no. 2 (August 1, 1993): 720–23. http://dx.doi.org/10.1152/jappl.1993.75.2.720.
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To characterize the changes in respiratory mechanics and ventilatory timing that accompany apnea in premature infants, we evaluated 36 apneas in 13 premature infants (birth weight, 1,200 +/- 350 g, postconceptional age at study 34 +/- 3 wk). Apnea was defined as a ventilatory pause > or = 10s accompanied by a decrease in heart rate of 20 beats/min. Nasal airflow was recorded with a pneumotachometer, and esophageal, pharyngeal, and nasal mask pressures were continuously measured. Inspiratory time (TI), expiratory time (TE), tidal volume (VT), and VT/TI were determined over five breaths before and after apnea. In addition, total pulmonary resistance (RT) and supraglottic resistance (Rs) were measured over the same epochs in inspiration and expiration. Before apnea, TE and RT increased (P < 0.05 and < 0.01, respectively); however, Rs did not change. Immediately after apnea, prolongation of TI occurred and both RT and Rs were increased (P < 0.01), consistent with continued upper airway instability. However, within two breaths after resolution of the apnea, RT and Rs returned to normal, reflecting rapid recovery of upper airway and total pulmonary resistance. The ventilatory changes that precede and follow apnea closely resemble those occurring during periodic breathing.
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Mattiuzzi, Camilla, Massimo Franchini, and Giuseppe Lippi. "Sleep apnea and venous thromboembolism." Thrombosis and Haemostasis 114, no. 11 (2015): 958–63. http://dx.doi.org/10.1160/th15-03-0188.
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SummaryRecent evidence suggests that obstructive sleep apnea is a significant and independent risk factor for a number of cardiovascular disorders. Since the association between obstructive sleep apnea and cardiovascular disease is mediated by endothelial dysfunction, hypercoagulability and platelet abnormalities, we sought to investigate whether sleep apnea may also be considered a risk factor for venous thromboembolism (VTE). We carried out an electronic search in Medline and Scopus using the keywords “apnea” OR “apnoea” AND “venous thromboembolism” OR “deep vein thrombosis” OR “pulmonary embolism” in “Title/Abstract/Keywords”, with no language or date restriction. Fifteen studies (8 case-control, 4 retrospective observational, 2 prospective case-control and 1 prospective observational) were finally selected for this systematic review. In all studies except one (14/15; 93%), obstructive sleep apnea was found to be an independent risk factor for VTE, either deep-vein thrombosis (DVT) or pulmonary embolism (PE). In the two prospective case-control studies the risk of DVT or PE was found to be two-to three-fold higher in patients with obstructive sleep apnea than in those without. In conclusion, the current epidemiological evidence supports the hypothesis that obstructive sleep apnea may be an independent risk factor for VTE.
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Wetmore, Stephen J., Lawrence Scrima, and F. Charles Hiller. "Sleep Apnea in Epistaxis Patients Treated with Nasal Packs." Otolaryngology–Head and Neck Surgery 98, no. 6 (June 1988): 596–99. http://dx.doi.org/10.1177/019459988809800611.
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The presence of anterior and posterior nasal packs in patients with epistaxis is known to be associated with cardiorespiratory problems and sometimes death, although the mechanism has not been well understood. To determine the incidence and severity of obstructive sleep apnea in patients with epistaxis treated with both anterior and posterior nasal packs, we obtained polysomnograms on twelve patients while the packs were in place. Ten of these patients demonstrated obstructive sleep apnea. The apnea index (apneas/hour sleep) ranged from 1 to 83, with a mean of 29; the hypopnea index (hypopneas/hour sleep) ranged from 9 to 33, with a mean of 20; and the lowest oxygen saturation (SaO2) ranged from 17% to 91%, with a mean of 77%. Ten patients returned for another polysomnogram after removal of the packs. These baseline studies showed improvement in the apnea index and in the lowest SaO2 in all patients, although four patients still demonstrated at least mild obstructive sleep apnea. This study demonstrates that nasal packs used for the treatment of epistaxis may induce obstructive sleep apnea or markedly exacerbate underlying obstructive sleep apnea and, therefore, contribute to the sudden deaths that have been reported in epistaxis patients.
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Hoiland, Ryan L., Philip N. Ainslie, Anthony R. Bain, David B. MacLeod, Mike Stembridge, Ivan Drvis, Dennis Madden, Otto Barak, Douglas M. MacLeod, and Zeljko Dujic. "β1-Blockade increases maximal apnea duration in elite breath-hold divers." Journal of Applied Physiology 122, no. 4 (April 1, 2017): 899–906. http://dx.doi.org/10.1152/japplphysiol.00127.2016.
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We hypothesized that the cardioselective β1-adrenoreceptor antagonist esmolol would improve maximal apnea duration in elite breath-hold divers. In elite national-level divers ( n = 9), maximal apneas were performed in a randomized and counterbalanced order while receiving either iv esmolol (150 μg·kg−1·min−1) or volume-matched saline (placebo). During apnea, heart rate (ECG), beat-by-beat blood pressure, stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were measured (finger photoplethysmography). Myocardial oxygen consumption (MV̇o2) was estimated from rate pressure product. Cerebral blood flow through the internal carotid (ICA) and vertebral arteries (VA) was assessed using Duplex ultrasound. Apnea duration improved in the esmolol trial when compared with placebo (356 ± 57 vs. 323 ± 61 s, P < 0.01) despite similar end-apnea peripheral oxyhemoglobin saturation (71.8 ± 10.3 vs. 74.9 ± 9.5%, P = 0.10). The HR response to apnea was reduced by esmolol at 10–30% of apnea duration, whereas MAP was unaffected. Esmolol reduced SV (main effect, P < 0.05) and CO (main effect; P < 0.05) and increased TPR (main effect, P < 0.05) throughout apnea. Esmolol also reduced MV̇o2 throughout apnea (main effect, P < 0.05). Cerebral blood flow through the ICA and VA was unchanged by esmolol at baseline and the last 30 s of apnea; however, global cerebral blood flow was reduced in the esmolol trial at end-apnea ( P < 0.05). Our findings demonstrate that, in elite breath-hold divers, apnea breakpoint is improved by β1-blockade, likely owing to an improved total body oxygen sparring through increased centralization of blood volume (↑TPR) and reduced MV̇o2. NEW & NOTEWORTHY The governing bodies for international apnea competition, the Association Internationale pour le Développment de l’Apnée and La Confédération Mondaile des Activités Subaquatiques, have banned the use of β-blockers based on anecdotal reports that they improve apnea duration. Using a randomized placebo-controlled trial, we are the first to empirically confirm that β-blockade improves apnea duration. This improvement in apnea duration coincided with a reduced myocardial oxygen consumption.
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Chen, Ling, and Steven M. Scharf. "Comparative hemodynamic effects of periodic obstructive and simulated central apneas in sedated pigs." Journal of Applied Physiology 83, no. 2 (August 1, 1997): 485–94. http://dx.doi.org/10.1152/jappl.1997.83.2.485.
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Chen, Ling, and Steven M. Scharf. Comparative hemodynamic effects of periodic obstructive and simulated central apneas in sedated pigs. J. Appl. Physiol. 83(2): 485–494, 1997.—It has been speculated that because of increased left ventricular (LV) afterload, decreased intrathoracic pressure (ITP) is responsible for decreased cardiac output (CO) in obstructive sleep apnea. If this were true, then obstructive apnea (OA) should have a greater effect on CO than would central apnea (CA). To assess the importance of decreased ITP during OA, we studied seven preinstrumented sedated pigs with OA and simulated CA that were matched for blood gases and apnea periodicities (with 15- or 30-s apnea duration). Compared with OA, CA with 30-s apnea duration produced comparable decreases in heart rate (from baseline to end apnea: OA, 106.6 ± 4.8 to 93.4 ± 4.4 beats/min, P < 0.01; and CA, 111.1 ± 6.2 to 94.0 ± 5.2 beats/min, P < 0.01) and comparable increases in LV end-diastolic pressure and LV end-diastolic myocardial segment length but greater increases in mean arterial pressure (97.1 ± 3.7 to 107.7 ± 4.3 Torr, P < 0.05; and 97.3 ± 4.8 to 119.3 ± 7.4 Torr, P < 0.01) and systemic vascular resistance (2,577 ± 224 to 3,346 ± 400 dyn ⋅ s ⋅ cm−5, P < 0.01; and 2,738 ± 294 to 5,111 ± 1,181 dyn ⋅ s ⋅ cm−5, P < 0.01) and greater decreases in CO (3.18 ± 0.31 to 2.74 ± 0.26 l/min, P < 0.05; and 3.07 ± 0.38 to 2.30 ± 0.36 l/min, P < 0.01) and stroke volume (32.2 ± 2.9 to 25.9 ± 2.4 ml, P < 0.05; and 31.5 ± 1.9 to 19.8 ± 3.1 ml, P < 0.01). Only CA increased LV end-systolic myocardial segment length. Similar findings were observed with 15-s apnea duration. We conclude that CA produced greater depression of CO and greater changes of afterload-related LV dysfunction than did OA. Therefore, decreased ITP was not the dominant factor determining LV function with apneas.
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Cutler, Michael J., Nicolette Muenter Swift, David M. Keller, Wendy L. Wasmund, and Michael L. Smith. "Hypoxia-mediated prolonged elevation of sympathetic nerve activity after periods of intermittent hypoxic apnea." Journal of Applied Physiology 96, no. 2 (February 2004): 754–61. http://dx.doi.org/10.1152/japplphysiol.00506.2003.
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Obstructive sleep apnea (OSA) is associated with transient elevation of muscle sympathetic nerve activity (MSNA) during apneic events, which often produces elevated daytime MSNA in OSA patients. Hypoxia is postulated to be the primary stimulus for elevated daytime MSNA in OSA patients. Therefore, we studied the effects of 20 min of intermittent voluntary hypoxic apneas on MSNA during 180 min of recovery. Also, we compared MSNA during recovery after either 20 min of intermittent voluntary hypoxic apneas, hypercapnic hypoxia, or isocapnic hypoxia. Consistent with our hypothesis, both total MSNA and MSNA burst frequency were elevated after 20 min of intermittent hypoxic apnea compared with baseline ( P < 0.05). Both total MSNA and MSNA burst frequency remained elevated throughout the 180-min recovery period and were statistically different from time control subjects throughout this period ( P < 0.05). Finally, MSNA during recovery from intermittent hypoxic apnea, hypercapnic hypoxia, and isocapnic hypoxia were not different ( P = 0.50). Therefore, these data support the hypothesis that short-term exposure to intermittent hypoxic apnea results in sustained elevation of MSNA and that hypoxia is the primary mediator of this response.
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Botelho, Ricardo Vieira, Lia Rita Azeredo Bittencourt, José Marcus Rotta, and Sérgio Tufik. "The effects of posterior fossa decompressive surgery in adult patients with Chiari malformation and sleep apnea." Journal of Neurosurgery 112, no. 4 (April 2010): 800–807. http://dx.doi.org/10.3171/2009.7.jns09174.
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Object One of the feared consequences of craniovertebral junction diseases is apnea. Although several cases of patients with central apnea have been described, obstructive sleep apnea has been identified as the most frequent manifestation of sleep respiratory disorder. Neuronal involvement may be responsible for both central and obstructive apneas. The objective of this work was to study the effect of posterior fossa decompressive surgery on respiratory parameters during sleep in patients with craniovertebral junction malformations and breathing-related sleep disorders. Methods In this study, prospectively enrolled consecutive symptomatic adult patients were monitored with full-night polysomnography before and after surgical decompression of the cranial posterior fossa. Results Of the 25 patients who were evaluated, 68% received a diagnosis of sleep apnea. After surgery, the mean number of respiratory events decreased from 180.70 to 69.29 (p = 0.005); the mean number of obstructive events decreased from 107.37 to 60.58 (p = 0.01); and the mean number of central events decreased from 38.45 to 8.05 (p = 0.01). The mean preoperative apnea/hypopnea index decreased from 26.68 to 12.98 (p = 0.06), and the mean central apnea index decreased from 13.81 to 1.68 (p = 0.01). Conclusions Decompressive surgery in patients with craniovertebral junction malformations resulted in decreased respiratory events during sleep, lowered sleep fragmentation, and enhanced the sleep apnea index in a significant number of patients. The effect was more pronounced in patients with central apnea.
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Durgan, David J., Randy F. Crossland, and Robert M. Bryan. "The rat cerebral vasculature exhibits time-of-day-dependent oscillations in circadian clock genes and vascular function that are attenuated following obstructive sleep apnea." Journal of Cerebral Blood Flow & Metabolism 37, no. 8 (January 1, 2016): 2806–19. http://dx.doi.org/10.1177/0271678x16675879.
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Circadian clock components oscillate in cells of the cardiovascular system. Disruption of these oscillations has been observed in cardiovascular diseases. We hypothesized that obstructive sleep apnea, which is associated with cerebrovascular diseases, disrupts the cerebrovascular circadian clock and rhythms in vascular function. Apneas were produced in rats during sleep. Following two weeks of sham or obstructive sleep apnea, cerebral arteries were isolated over 24 h for mRNA and functional analysis. mRNA expression of clock genes exhibited 24-h rhythms in cerebral arteries of sham rats (p < 0.05). Interestingly, peak expression of clock genes was significantly lower following obstructive sleep apnea (p < 0.05). Obstructive sleep apnea did not alter clock genes in the heart, or rhythms in locomotor activity. Isolated posterior cerebral arteries from sham rats exhibited a diurnal rhythm in sensitivity to luminally applied ATP, being most responsive at the beginning of the active phase (p < 0.05). This rhythm was absent in arteries from obstructive sleep apnea rats (p < 0.05). Rhythms in ATP sensitivity in sham vessels were absent, and not different from obstructive sleep apnea, following treatment with L-NAME and indomethacin. We conclude that cerebral arteries possess a functional circadian clock and exhibit a diurnal rhythm in vasoreactivity to ATP. Obstructive sleep apnea attenuates these rhythms in cerebral arteries, potentially contributing to obstructive sleep apnea-associated cerebrovascular disease.