central apnea
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2021 ◽  
Vol 8 ◽  
Author(s):  
Gian Domenico Pinna ◽  
Elena Robbi ◽  
Claudio Bruschi ◽  
Maria Teresa La Rovere ◽  
Roberto Maestri

Study Objectives: Arousals from sleep during the hyperpneic phases of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with heart failure are thought to cause ventilatory overshoot and a consequent longer apnea, thereby sustaining and exacerbating ventilatory instability. However, data supporting this model are lacking. We investigated the relationship between arousals, hyperpnea and post-hyperpnea apnea length during CSR-CSA.Methods: Breath-by-breath changes in ventilation associated with the occurrence of arousal were evaluated in 18 heart failure patients with CSR-CSA, apnea-hypopnea index ≥15/h and central apnea index ≥5/h. The change in apnea length associated with the presence of arousal during the previous hyperpnea was also evaluated. Potential confounding variables (chemical drive, sleep stage) were controlled for.Results: Arousals were associated with a large increase in ventilation at the beginning of the hyperpnea (+76 ± 35%, p < 0.0001), that rapidly declined during its crescendo phase. Around peak hyperpnea, the change in ventilation was −8 ± 26% (p = 0.14). The presence of arousal during the hyperpnea was associated with a median increase in the length of the subsequent apnea of +4.6% (Q1, Q2: −0.7%, 20.5%; range: −8.5%, 36.2%) (p = 0.021). The incidence of arousals occurring at the beginning of hyperpnea and mean ventilation in the region around its peak were independent predictors of the change in apnea length (p = 0.004 and p = 0.015, respectively; R2 = 0.78).Conclusions: Arousals from sleep during CSR-CSA in heart failure patients are associated with a rapidly decreasing ventilatory overshoot at the beginning of the hyperpnea, followed by a tendency toward a slight ventilatory undershoot around its peak. On average, arousals are also associated with a modest increase in post-hyperpnea apnea length; however, large increases in apnea length (>20%) occur in about a quarter of the patients.


2021 ◽  
Vol 12 ◽  
Author(s):  
Elisa Micalizzi ◽  
Anna Elisabetta Vaudano ◽  
Giada Giovannini ◽  
Giulia Turchi ◽  
Leandra Giunta ◽  
...  

Ictal respiratory changes have been mainly described following generalized tonic-clonic seizures and recently considered to be a biomarker to assess the risk of sudden unexplained death in epilepsy (SUDEP). Nonetheless, modification of respiratory pattern can be related also to focal seizures, especially arising from the temporal lobe. Changes in cardiac function such as tachycardia or bradycardia could be often associated. We report a short case series of four patients with temporal lobe epilepsy admitted to our Epilepsy Monitoring Unit (EMU) presenting with an ictal central apnea as the first clinical manifestation of their seizures. None of these patients was aware of the occurrence of respiratory arrest. Age at onset ranged from 15 to 29 years. One patient had seizures with prolonged central apnea accompanied by a significant decrease in oxygen saturation. Neuroimaging in two patients showed alterations of mesial temporal lobe structures, including the amygdala. Recent neurophysiological studies supported the existence of a cortical network involving the limbic system that modulates downstream brainstem respiratory centers. Monitoring for respiratory changes and oxygen saturation in focal seizures is warranted for their potential value in identifying the epileptogenic zone and for a better understanding of ictal respiratory changes that could potentially define a subgroup of patients with high risk of seizure-related autonomic changes.


2021 ◽  
Author(s):  
Olabimpe S Fashanu ◽  
Stuart F Quan

Objectives: To determine factors that predict OSA therapy outcomes with auto-titrating positive airway pressure (APAP). Methods: We sequentially grouped patients from a retrospective cohort based on APAP efficacy (sufficiently vs. insufficiently treated; insufficiently treatment defined as residual AHI of > 5); therapy adherence (compliant vs. non-compliant, non-compliance defined as < 70% usage for ≥ 4 hours/night); and therapy outcomes (optimal vs non-optimal (non-optimal outcomes defined as non-compliant and insufficiently treated). We subsequently compared each group. Results: The insufficiently treated were older (68.4 ± 12.5 vs. 60.4 ± 13.1 years, p < 0.01) and had lower BMI (31.9 ± 6.3 vs.37.9 ± 9.1 kg/m2, p < 0.01). They had higher baseline central apnea indices (CAI), longer leaks, higher peak pressures and were less compliant. The non-compliant were younger (61.1 ±12.6 vs. 65.5 ± years, p = 0.03) and comprised more females (56.1 vs. 43.9%, p = 0.04). The leak duration per usage hour was higher in the non-compliant (13.9 ±42.1 vs. 1.83 ±3.53 minutes/hour, p < 0.01). The non-optimally treated had lower BMI , longer leaks and shorter nightly usage. Following multivariate analysis, the aforementioned variables except age were predictive of higher residual AHI, while age and gender predicted compliance. Conclusions: Various demographic and clinical factors were predictive of treatment efficacy and adherence. Overall, lower BMI, longer leaks and shorter nightly usage predicted poor therapy outcomes.


2021 ◽  
Author(s):  
María José Abenza Abildúa ◽  
Vanesa Lores Gutiérrez ◽  
Javier Giner García ◽  
Francisco José Navacerrada Barrero ◽  
Beatriz Sánchez García ◽  
...  

2021 ◽  
Author(s):  
Sergio Ghirardo ◽  
Alessandro Amaddeo ◽  
Lucie Griffon ◽  
Sonia Khirani ◽  
Brigitte Fauroux

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A187-A187
Author(s):  
Eline Oppersma ◽  
Wolfgang Ganglberger ◽  
Haoqi Sun ◽  
Robert Thomas ◽  
Michael Westover

Abstract Introduction Sleep disordered breathing is a significant risk factor for cardiometabolic and neurodegenerative diseases. Tolerance and efficacy of continuous positive airway pressure (CPAP), the primary form of therapy for sleep apnea, is often poor. High loop gain (HLG) is a driving mechanism of central sleep apnea or periodic breathing. The current study aimed to develop a computational approach to detect HLG based on self-similarity in respiratory oscillations during sleep solely using breathing patterns, measured via Respiratory Inductance Plethysmography (RIP). To quantify the potential utility of the developed similarity metric, the presented algorithm was used to predict acute CPAP failure. Methods We developed an algorithm for detecting apneas as periods with reduced breathing effort, manifested in the RIP signal as low signal amplitude. Our algorithm calculates self-similarity in breathing patterns between consecutive periods of apnea or hypopnea. Working under the assumption that high loop gain induces self-similar respiratory oscillations and increases the risk of failure during CPAP, the full night similarity, computed during diagnostic non-CPAP polysomnography (PSG), was used to predict failure of CPAP, which we defined as titration central apnea index (CAI)&gt;10. Central apnea labels are obtained both from manual scoring by sleep technologists, and from an automated algorithm developed for this study. The Massachusetts General Hospital (MGH) sleep database was used, including 2466 PSG pairs of diagnostic and CPAP titration PSG recordings. Results Diagnostic CAI based on technologist labels predicted failure of CPAP with an AUC of 0.82 ±0.03. Based on automatically generated labels, the combination of full night similarity and automatically generated CAI resulted in an AUC of 0.85 ±0.02. A subanalysis was performed on a population with technologist labeled diagnostic CAI&gt;5. Full night similarity predicted failure with an AUC of 0.57 ±0.07 for manual and 0.65 ±0.06 for automated labels. Conclusion This study showed that central apnea labels can be derived in an automated way. The proposed self-similarity feature, as a surrogate estimate of expressed respiratory high loop gain and computed from easily accessible effort signals, can detect periodic breathing regardless of admixed obstructive features such as flow-limitation, and can aid prediction of CPAP failure or success. Support (if any):


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A322-A322
Author(s):  
Jared Colvert ◽  
Glen Greenough

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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