Cessation in airflow of 10 or more seconds in the absence of any inspiratory effort.
CSA is diagnosed when ≥ 50% of events are central.
Classification
International Classification of Sleep Disorders, 2nd edition (ICSD-2):
Primary (idiopathic) CSA
Cheyne-Stokes breathing (CSB) pattern
CSA due to high-altitude periodic breathing
CSA due to drug/substance
Primary sleep apnoea of infancy
Complex sleep apnoea (complex SA):
Primarily OSA/mixed apnoeas who develop central apnoeas on positive airway pressure (PAP) treatment (treatment-emergent central apnoeas) or have significant persistent central apnoeas on PAP treatment (treatment-persistent CSAs).
Hypocapnic CSA:
Normal/low wake PaCO2 and do not develop sleep hypercapnoea.
Includes:
Primary (idiopathic) CSA (ICSA)
Cheyne-Stokes breathing (CSB) pattern
Complex CSA
Hypercapnic CSA:
High normal/elevated wake PaCO2 (may rise further in sleep)
Opium: depress respiratory center in a dose-dependent manner.
Barbiturates: cause respiratory depression in high doses
Gelsemium: This is an ergot-type alkaloid and is a CNS depressant. With large doses, paralysis and death from respiratory failure can occur.
Complications
Heart failure:
Pathophysiologic Consequences of CSA in Heart Failure: The repeated episodes of apnea, hypoxia, reoxygenation, and arousal throughout the night are the factors leading to the pathophysiologic consequences of central sleep apnea (CSA). These pathologic effects are multiple, and include sympathetic nervous system activation, oxidative stress, systemic inflammation, and endothelial dysfunction. All contribute to worsening heart failure. RAAS = renin-angiotensin aldosterone system. | Costanzo, M. R., Khayat, R., Ponikowski, P., Augostini, R., Stellbrink, C., Mianulli, M., & Abraham, W. T. (2015). Mechanisms and clinical consequences of untreated central sleep apnea in heart failure. Journal of the American College of Cardiology, 65(1), 72–84. https://doi.org/10.1016/j.jacc.2014.10.025
Diagnosis
Polysomnography: multi-parametric test and includes:
EEG
Eye movements (EOG)
Skeletal muscle activation (EMG)
ECG
Respiratory airflow and respiratory effort indicators
Peripheral pulse oximetry
Sleep latency
Sleep efficiency
Arousal index
Top, A: An example of a patient receiving high-dose opioid medication for back pain experiencing repetitive central apneas as demonstrated by a lack of movement of respiratory effort bands (both abdominal and thoracic) with associated oxygen desaturations. Bottom, B: Marked improvement in SDB following gradual dose reduction of opioid medication. Sao2 = arterial oxygen saturation | Eckert, D. J., Jordan, A. S., Merchia, P., & Malhotra, A. (2007). Central sleep apnea: Pathophysiology and treatment. Chest, 131(2), 595–607. https://doi.org/10.1378/chest.06.2287
An example of a patient with CSB. Note the characteristic crescendo/decrescendo pattern of breathing, long circulation time (each oxygen desaturation corresponds to the previous apnea), and arousal occurring at the peak of respiratory effort.. Sao2 = arterial oxygen saturation | Eckert, D. J., Jordan, A. S., Merchia, P., & Malhotra, A. (2007). Central sleep apnea: Pathophysiology and treatment. Chest, 131(2), 595–607. https://doi.org/10.1378/chest.06.2287
An example of ICSA. Note the shortened cycle time (approximately 25 s in this example) compared to CSB and that arousal (arrow) occurs at the cessation of apnea. | Malhotra A, Berry RB, White DP. Central sleep apnea. In: Carney PR, Berry RB, Geyer JD, editors. Clinical sleep disorders. Philadelphia, PA: Lippincott Williams and Wilkins; 2004. pp. 331–346
Polysomnogram of CSA in a Patient With Heart Failure: Overnight polysomnography performed in a sleep laboratory remains the gold standard for diagnosing sleep-disordered breathing. The image highlights characteristic findings of central sleep apnea (CSA) on a polysomnogram. | Costanzo, M. R., Khayat, R., Ponikowski, P., Augostini, R., Stellbrink, C., Mianulli, M., & Abraham, W. T. (2015). Mechanisms and clinical consequences of untreated central sleep apnea in heart failure. Journal of the American College of Cardiology, 65(1), 72–84. https://doi.org/10.1016/j.jacc.2014.10.025
Management
Continuous Positive Airway Pressure (CPAP):
Haemodynamic effects:
↑ right atrial pressure
↓ cardiac pre-load
↑ oxygenation
↓ catecholamines
↓ ventricular wall tension/after-load
Improved mitral regurgitation
↓ pleural pressure required for inspiration by improving lung compliance
Improved right-ventricular after-load through ↓ pulmonary vasoconstriction from hypoxemia and catecholamines
Form of closed-loop mechanical ventilation, pressure preset, and volume or flow cycled. Alleviates central sleep apnea due to CSBP by providing dynamic (breath-by-breath) adjustment of inspiratory pressure support with a back-up rate to normalize breathing patterns relative to a predetermined target. Specifically, ASV mitigates hyperventilation and associated hypocapnia by delivering preset minute ventilation.
Csa secondary to heart failure: Nocturnal oxygen therapy
Practical CSA Management in Patients With Heart Failure: Current treatment strategies for central sleep apnea (CSA) focus on either improving heart failure (HF) or reducing CSA itself. ACE-I = angiotensin-converting enzyme inhibitor; OSA = obstructive sleep apnea; SDB = sleep-disordered breathing; Sxs = symptoms. | Costanzo, M. R., Khayat, R., Ponikowski, P., Augostini, R., Stellbrink, C., Mianulli, M., & Abraham, W. T. (2015). Mechanisms and clinical consequences of untreated central sleep apnea in heart failure. Journal of the American College of Cardiology, 65(1), 72–84. https://doi.org/10.1016/j.jacc.2014.10.025
