AN EFFECTIVE TITRATION STUDY IS AN INTERPLAY BETWEEN PATIENT, SLEEP TECHNICIAN, INTERFACE AND OPTIMAL PRESSURE

CHEST Journal ◽  
2021 ◽  
Vol 160 (4) ◽  
pp. A2404
Author(s):  
Anoop Narahari ◽  
Neal Patel ◽  
Brendon Colaco ◽  
Vichaya Arunthari
Keyword(s):  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Kathryn A. Ryan ◽  
Kevin R. Bewley ◽  
Susan A. Fotheringham ◽  
Gillian S. Slack ◽  
Phillip Brown ◽  
...  

AbstractThere is a vital need for authentic COVID-19 animal models to enable the pre-clinical evaluation of candidate vaccines and therapeutics. Here we report a dose titration study of SARS-CoV-2 in the ferret model. After a high (5 × 106 pfu) and medium (5 × 104 pfu) dose of virus is delivered, intranasally, viral RNA shedding in the upper respiratory tract (URT) is observed in 6/6 animals, however, only 1/6 ferrets show similar signs after low dose (5 × 102 pfu) challenge. Following sequential culls pathological signs of mild multifocal bronchopneumonia in approximately 5–15% of the lung is seen on day 3, in high and medium dosed groups. Ferrets re-challenged, after virus shedding ceased, are fully protected from acute lung pathology. The endpoints of URT viral RNA replication & distinct lung pathology are observed most consistently in the high dose group. This ferret model of SARS-CoV-2 infection presents a mild clinical disease.


1991 ◽  
Vol 1 (3) ◽  
pp. 438
Author(s):  
C Geretsegger ◽  
G.F Hebenstreit ◽  
C Stuppäck ◽  
P König ◽  
H Schubert ◽  
...  

1988 ◽  
Vol 61 (2) ◽  
pp. 407-411 ◽  
Author(s):  
Kenta Ooi ◽  
Yoshitaka Miyai ◽  
Shunsaku Katoh ◽  
Hiroshi Maeda ◽  
Mitsuo Abe

2003 ◽  
Vol 19 (5) ◽  
pp. 775-777
Author(s):  
Kiyoharu NAKATANI ◽  
Jun YAMASHITA ◽  
Tomomi SEKINE ◽  
Minoru TORIUMI ◽  
Toshiro ITANI

1975 ◽  
Vol 78 (6) ◽  
pp. 1241-1246
Author(s):  
Toshihiko OKUDA ◽  
Shintaro SUGAI
Keyword(s):  

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A328-A328
Author(s):  
Jessica Cho ◽  
David Dai ◽  
Constance Fung

Abstract Introduction We present a case of paradoxically worsened hypoxia during wake phase of polysomnography while undergoing a CPAP titration study. Nighttime hypoxemia is a common feature in obstructive sleep apnea, due to obstructive events that manifest while sleeping. Excluding OSA, there remains an extensive differential for disease processes that cause hypoxemia while asleep; however, none of these processes can explain waking hypoxemia that improves upon sleeping. Report of case(s) A 70 year old male with severe OSA diagnosed by home sleep test (REI 46.5, nadir O2=76%) underwent polysomnography with PAP titration and demonstrated several hours of interrupted sleep without hypoxia and minimal obstructive events on CPAP 9–13 cmH2O. During the study, while awake at CPAP of 14 cmH2O, he developed hypoxia to mid-high 80s and supplemental oxygen bleed in was added starting at 3L and increased to 5L during a prolonged period of wakefulness. On CPAP 15 cmmH2O with 5L bleed-in, the patient fell asleep and oxygen saturation again increased to low 90s. He underwent an extensive workup for other cardiopulmonary causes of hypoxemia, with pulmonary function testing showing moderate obstructive ventilatory defect and mild DLCO impairment. An echocardiogram with saline contrast bubble study was relatively unremarkable, without evidence of right to left shunting. He underwent a chest CTA which was negative for pulmonary embolism, though it did reveal an enlarged pulmonary artery consistent with pulmonary hypertension. His chronic hypoxemia was treated with 2L supplemental oxygen during the day and bleed-in with CPAP at night. Conclusion Though nocturnal hypoxemia is common with OSA, polysomnography with paradoxical hypoxemia during wake phase has not been reported. Notably, the patient was without prolonged hypoxia during his sleep phase while on CPAP treatment with minimal apneic/hypopneic events. Pulmonary hypertension can also present as nocturnal hypoxemia, but it should worsen with sleep, rather than improve. There are case reports of right to left shunting worsened by PAP, though his hypoxemia persisted despite PAP. His paradoxical worsening hypoxemia with wakefulness is still unexplained. Support (if any):


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A470-A471
Author(s):  
Ugorji Okorie ◽  
Brittany Monceaux ◽  
Megan Smalley ◽  
Edmond Roberts ◽  
Cesar Liendo ◽  
...  

Abstract Introduction No standard of care exists for management of sleep disorders/sleep disordered breathing (SDB) and Mitochondrial myopathies. Our case report describes our experience with this condition in a pediatric patient. Report of Case A ten-year-old middle eastern male with PMH of Mitochondrial myopathy was referred to Sleep Medicine by ENT with reported snoring, witnessed apneic spells and daytime fatigue. Flexible Video Laryngoscopy did not reveal tonsillar or adenoid hypertrophy so it was postulated that his OSA was a result of his craniofacial abnormalities and global hypotonia. Genetic workup showed Mitochondrial complex II & III deficiency from a variant in SNAPC4 gene and PURA gene leading to failure to thrive, severe developmental delay, generalized muscle weakness, bradycardia requiring pacemaker, global hypotonia requiring nocturnal oxygen for chronic respiratory failure and G-tube placement due to difficulty with feedings. Diagnostic PSG showed severe OSA with AHI of 11.3, RDI 11.8, REM AHI 56.0, REM RDI 56, and minimum oxygen saturation 85%. Subsequent PAP titration led to initiation of BIPAP therapy with settings of Auto-BiPAP EPAP min 5, IPAP max 20; PSmin 4; PSmax 6 cm H2O and continuation of nocturnal home oxygen. Sleep fragmentation improved to an arousal index of 3.1 with BIPAP. The patient and caregiver presented to the Sleep Medicine clinic 1 month after the PAP titration study with objective report showing >4 hours use >70% of the time and subjective satisfaction with BIPAP therapy with improvement in snoring and apnea. Conclusion Mitochondrial disorders lead to a deficiency of ATP affecting all organ systems and is most recognizable in the form of neuromuscular impairments. Neuromuscular impairments can translate into SDB issues such as OSA. Patients with genetic conditions such as mitochondrial myopathy should be routinely screened and evaluated for SDB and treated if warranted to significantly improve morbidity, mortality and quality of life.


1990 ◽  
Vol 137 (9) ◽  
pp. 2962-2966
Author(s):  
A. Vervaet ◽  
I. Clemminck ◽  
M. Burgelman

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