Cheyne-Stokes respiration medical therapy

Cheyne-Stokes respiration Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Cheyne-Stokes respiration from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Cheyne-Stokes respiration medical therapy On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Cheyne-Stokes respiration medical therapy All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Cheyne-Stokes respiration medical therapy
CDC on Cheyne-Stokes respiration medical therapy
Cheyne-Stokes respiration medical therapy in the news
Blogs on Cheyne-Stokes respiration medical therapy
Directions to Hospitals Treating Cheyne-Stokes respiration
Risk calculators and risk factors for Cheyne-Stokes respiration medical therapy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Medical Therapy

Obviously, CHF is associated with an increased mortality. The data concerning CSR and mortality is equivocal. It is unclear if CSR actually increases mortality from CHF (which would make physiologic sense), or is just a marker of more severe disease.

It has been shown that CSR can resolve in a majority of patients with adequate treatment of the underlying CHF.

• ACE inhibitors have been associated with a 50% reduction in the frequency of apnea and desaturation in patients with class II – III CHF. The exact mechanism remains unknown, but improved circulatory time is a leading contender.
• Nocturnal oxygen (2-3 L/min) has been shown to reduce the duration of CSR, improve hypoxemia, sleep, and daytime cognitive function patients with severe CHF. The long term effects of nocturnal oxygen in these patients, however, remain unproven.

  • Low-flow oxygen was also found to reverse both CSR and desaturations in patients with acute strokes.
  • It is felt that eliminating hypoxemia reduces the gain of the respiratory control system. It also reduces respiratory drive, thus resulting in an increase in PaCO2 as well.

• One study showed that 3.3 mg/kg of theophylline bid reduced the AHI (from 37 to 18), and duration of sleep with SaO2 < 90% (23% vs. 6%) in patients with CHF / obstructive sleep apnea (OSA).

  • Theophylline has also been shown to reverse CSR and desaturation in patients with acute stroke.

• Another study found that administering 3% CO2 to 6 patients with CHF and CSR reduced the duration of CSR from 62% to 2.2% of sleep time.
• The mechanisms by which continuous positive airway pressure (CPAP) improves central sleep apnea (CSA) in patients with CHF are likely multifactorial.

  • By increasing functional residual capacity (FRC), and therefore intrathoracic pressure, afterload and preload are reduced, and cardiac output increases. This results in a shorter circulation time. In patients with low filling pressures, however, the decrease in preload can reduce cardiac output.

    • Several studies have shown improvement in [NYHA classification]] in patients with CHF/CSR, and with CHF alone, who were treated with CPAP.
    • Additionally, Naughton et.al. showed that nasal CPAP caused an increase in left ventricular ejection fraction (LVEF), a decrease in heart rate (HR), and an increase in quality of life, as measured by dyspnea, fatigue, emotional well being and disease mastery.

  • CPAP, usually in pressures of 8 – 12 cm H20, can also eliminate apneas (and therefore arousals), as well as desaturations. The reduction in sympathetic tone may be another mechanism for improved CHF.
  • By increasing PaO2, the gain of the system is reduced (as above).
  • CPAP can also increase the PaCO2. The mechanism of this is likely multifactorial, and includes a reduction in ventilatory effort caused by improvement in pulmonary edema, a reduction in arousal mediated hyperventilation, and by reducing the gain of the ventilatory system by increasing PaO2.

    • This may drive the PaCO2 over the apnea threshold. Additionally, increased body CO2 stores can help buffer transient changes in PaCO2.

  • Unfortunately, there are no good studies that recommend using sleep studies in the routine evaluation of CHF. However, if a patients CHF is maximally treated, preliminary data would suggest performing sleep studies in patients with signs and symptoms of obstructive sleep apnea (OSA), CSR and possibly in patients with nocturnal angina or arrhythmia.