Treatment of refractory sleep apnea with supplemental carbon dioxide.

Badr, M. Safwan; Grossman, Jacob; Weber, Silke Anna Thereza

doi:10.1164/ajrccm.150.2.8049848

Cited by 53 publications

(28 citation statements)

References 11 publications

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“…This patient was treated successfully with supplemental CO 2 therapy [100]. This case report illustrates many fundamental aspects of the problem of central sleep apnoea.…”

Section: Normocapnic Patientsmentioning

confidence: 75%

Central sleep apnoea, pathogenesis and treatment: an overview and perspective

Backer

1995

Eur Respir J

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C Ce en nt tr ra al l s sl le ee ep p a ap pn no oe ea a, , p pa at th ho og ge en ne es si is s a an nd d t tr re ea at tm me en nt t: : a an n o ov ve er rv vi ie ew w a an nd d p pe er rs sp pe ec ct ti iv ve e There is accumulating evidence that central sleep apnoea should be considered as the end of a spectrum. Instability in the breathing pattern is the main underlying mechanism and is due to the interaction of many factors. Breathing during sleep is dependent on metabolic control and the activity of the respiratory muscles. Treatment strategies are remarkably few in number. Use of nasal ventilation and the inhalation of CO 2 are mainly of theoretical interest, since patients do not often tolerate these more invasive therapies. Drug treatment, especially with acetazolamide, is easier to perform. Stimulation of upper airway reflexes, by less invasive methods, seems to be promising for the near future.

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“…This patient was treated successfully with supplemental CO 2 therapy [100]. This case report illustrates many fundamental aspects of the problem of central sleep apnoea.…”

Section: Normocapnic Patientsmentioning

confidence: 75%

Central sleep apnoea, pathogenesis and treatment: an overview and perspective

Backer

1995

Eur Respir J

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“…Furthermore, when PSV was used in sleeping humans to increase VT sufficiently to reduce PET CO 2 below the apneic threshold, two PSV breaths (or 10-12 s) were sufficient to cause apnea (46). Finally, increased FI CO 2 in sleeping humans with PB was shown to eliminate apnea within 10-15 s of the onset of its application (3,7,47).…”

Section: Discussionmentioning

confidence: 89%

“…For changes in arterial pH, we assumed that the dogs' blood buffer slopes were parallel to the normal human blood buffer slope and passed through the measured eupneic Pa CO 2 -pH point determined for each dog on each day. Changes in cerebrospinal fluid (CSF) pH for a given change in ⌬PET CO 2 between eupnea and apnea were estimated by assuming no change in CSF HCO 3 Ϫ concentration ([HCO 3 Ϫ ]). We also assumed that CSF [HCO 3 Ϫ ] was equal to the measured eupneic arterial [HCO 3 Ϫ ] measured on that day, that CSF PCO2 was equal to PETCO 2 ϩ 6 Torr (41), and that ⌬PETCO 2 equaled the change in CSF PCO2.…”

Section: For Details)mentioning

confidence: 99%

Carotid body denervation eliminates apnea in response to transient hypocapnia

Nakayama¹,

Smith²,

Rodman³

et al. 2003

Journal of Applied Physiology

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“…Data on sleep or cardiac function were, however, not reported. BADR et al [18] described the ef-fects of inhaled 2% CO 2 in a patient with persistent central sleep apnoea after being treated with tracheostomy for obstructive sleep apnoea. Similarly to a recent case report [19], central apnoeas were suspended and sleep architecture was improved.…”

Section: Discussionmentioning

confidence: 99%

Treatment of Cheyne-Stokes respiration with nasal oxygen and carbon dioxide

Andreas

Weidel²,

Hagenah³

et al. 1998

Eur Respir J

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Cheyne-Stokes respiration (CSR) during sleep is common in patients with severe congestive heart failure (CHF). It induces repetitive oxygen desaturations and impairs sleep [1,2]. Disturbed sleep is likely to cause daytime symptoms and the repetitive oxygen desaturations and arousals increase sympathetic activity as well as right and left ventricular afterload [3] and may thus further impede left ventricular function and exercise tolerance [4][5][6]. Effective treatment for CSR is therefore needed. Nocturnal oxygen by nasal prongs reduces CSR by about 50% and consolidates sleep [1,[6][7][8]. Application of 3% CO 2 prevented CSR by increasing the arterial carbon dioxide tension (Pa,CO 2 ) above the apnoeic threshold [9] but sleep was adversely affected, this being attributed to the tight-fitting face mask used [10]. The hypothesis was tested that CO 2 in conjunction with O 2 given by nasal prongs is efficacious in the treatment of CSR. Plasma catecholamines were measured, to evaluate possible effects on sympathetic activity. Methods Subjects and protocolAll patients with severe heart failure admitted to the department of cardiology were candidates for the study.Patients under the age of 75 yrs were eligible if they met the following criteria: at least one episode of cardiac decompensation, ejection fraction ð35%, stable condition on cardiac medication and evidence of CSR by nocturnal polysomnography. Exclusion criteria were myocardial infarction within 1 yr of entry, significant obstructive lung disease as defined by a forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) <70%, primary valvular heart disease, tibial oedema or evidence of obstructive sleep apnoea (more than five obstructive apnoeas·h -1 ). Plasma catecholamines were evaluated in 15 healthy subjects (age 53.2±5.3 yrs) without significant sleep-disordered breathing. The study was approved by the local ethics committee. Informed written consent was obtained from all subjects.The study was designed as a single-blind, placebo-controlled trial. After an accommodation night where no treatment was applied the patients received air as well as O 2 plus CO 2 in a randomized, cross-over fashion on two consecutive nights. Polysomnography was performed during all three nights. Oxygen was given with a flow rate of 2 L·min -1 by nasal prongs and CO 2 was admixed simultaneously with a flow rate of 0.2-1 L·min -1 . Accordingly, the flow rate of the mixture was 2.2-3 L·min -1 . CO 2 flow rate was regulated depending on the transcutaneous carbon dioxide tension (Ptc,CO 2 ), which was not allowed to increase >7.3 kPa (55 mmHg) and on the occurrence of In conclusion, nocturnal O 2 plus CO 2 improves Cheyne-Stokes respiration in patients with congestive heart failure but has adverse effects on the sequel of CheyneStokes respiration, namely sympathetic activation. Eur Respir J 1998; 12: 414-419.

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Treatment of refractory sleep apnea with supplemental carbon dioxide.

Cited by 53 publications

References 11 publications

Central sleep apnoea, pathogenesis and treatment: an overview and perspective

Central sleep apnoea, pathogenesis and treatment: an overview and perspective

Carotid body denervation eliminates apnea in response to transient hypocapnia

Treatment of Cheyne-Stokes respiration with nasal oxygen and carbon dioxide

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