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. 2018 Jun 15;14(6):915-921.
doi: 10.5664/jcsm.7148.

CON: Persistent Central Sleep Apnea/Hunter-Cheyne-Stokes Breathing, Despite Best Guideline-Based Therapy of Heart Failure With Reduced Ejection Fraction, Is Not a Compensatory Mechanism and Should Be Suppressed

Affiliations

CON: Persistent Central Sleep Apnea/Hunter-Cheyne-Stokes Breathing, Despite Best Guideline-Based Therapy of Heart Failure With Reduced Ejection Fraction, Is Not a Compensatory Mechanism and Should Be Suppressed

Shahrokh Javaheri et al. J Clin Sleep Med. .
No abstract available

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Figures

Figure 1
Figure 1. Work of breathing with central apnea.
A 30-second epoch of central sleep apnea (CSA). From top to bottom: 2 channels of electro-oculogram (EOG), chin electromyogram (CHIN EMG), 2 channels of electroencephalogram (EEG), electrocardiogram (EKG), airflow (CO2), rib cage (RC) and abdominal (ABD) sum as well as in separate channels, esophageal pressure (PES), and oxyhemoglobin saturation (SaO2) measured by pulse oximetry. Note absence of airflow, and excursions in pleural pressure, thorax, and abdomen with CSA when work of breathing should be zero. However, following CSA there is hyperventilation with relatively large negative swings in esophageal pressure with hyperventilation which should increase WOB. Reprinted with permission of the American Thoracic Society. Copyright © 2018 American Thoracic Society. Modified from Dowdell WT, Javaheri S, McGinnis W. Cheyne-Stokes respiration presenting as sleep apnea syndrome: clinical and polysomnographic features. Am Rev Respir Dis. 1990;141:871–879. The American Review of Respiratory Disease is an official journal of the American Thoracic Society.
Figure 2
Figure 2. Heart failure with reduced ejection fraction is a hyperadrenergic state.
There are multiple mechanisms contributing to increased sympathetic activity, and presence of CSA further contributes. Locus coeruleus is the brainstem arousal network, and norepinephrine is the neurotransmitter. Modified and reprinted from Journal of the American College of Cardiology, Vol. 69, 2017, Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea types, mechanisms, and clinical cardiovascular consequences, pages 841–858, © 2018, with permission from Elsevier.
Figure 3
Figure 3. Work of breathing with obstructive apnea
An epoch of polysomnogram showing obstructive sleep apnea (OSA). Channels as in Figure 1 except absence of electro-oculogram. During OSA, there is progressive decrease in esophageal pressure against a closed upper airway, increasing work of breathing, which should diminish as the upper airway opens and pressure swings diminish.
Figure 4
Figure 4. Work of breathing with periodic breathing.
Work of breathing (WOB, Y axis on theft) measured in 25 patients with HFrEF while they exhibited normal breathing or periods of obstructive or central sleep apnea, showing that WOB is equally increased in sleep apnea compared to normal breathing. However, pressure time product was lower with central sleep apnea (Y axis on the right). Reprinted with permission of the American Thoracic Society. Copyright © 2018 American Thoracic Society. Modified from Kee K, Sands SA, Stuart-Andrews, et al. Effect of apnea type on work of breathing and respiratory fatigability during sleep in humans with heart failure [abstract]. Am J Respir Crit Care Med. 2014;189:A3892. The American Journal of Respiratory and Critical Care Medicine is an official journal of the American Thoracic Society.

Comment in

  • Rebuttal to Javaheri, Brown and Khayat.
    Naughton MT. Naughton MT. J Clin Sleep Med. 2018 Jun 15;14(6):927-929. doi: 10.5664/jcsm.7152. J Clin Sleep Med. 2018. PMID: 29852918 Free PMC article. No abstract available.
  • Rebuttal to Naughton.
    Javaheri S, Brown LK, Khayat R. Javaheri S, et al. J Clin Sleep Med. 2018 Jun 15;14(6):923-925. doi: 10.5664/jcsm.7150. J Clin Sleep Med. 2018. PMID: 29852919 Free PMC article. No abstract available.

References

    1. Javaheri S, Barbe F, Campos-Rodriguez F, et al. Sleep apnea types, mechanisms, and clinical cardiovascular consequences. J Am Coll Cardiol. 2017;69(7):841–858. - PMC - PubMed
    1. Naughton MT. Cheyne-Stokes respiration: friend or foe? Thorax. 2012;67(4):357–360. - PubMed
    1. Cowie MR, Woehrle H, Wegscheider K, et al. Adaptive servo-ventilation for central sleep apnea in systolic heart failure. N Engl J Med. 2015;373(12):1095–1105. - PMC - PubMed
    1. Javaheri S, Brown LK, Randerath W, Khayat R. SERVE-HF: more questions than answers [commentary] Chest. 2016;149(4):900–904. - PubMed
    1. Brack T, Jubran A, Laghi F, et al. Fluctuations in end-expiratory lung volume during Cheyne-Stokes respiration. Am J Respir Crit Care Med. 2005;171(12):1408–1413. - PubMed

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