Author:
Editor(s):
Updated:
ULY CLINIC
ULY CLINIC
25 Mei 2025, 10:49:13
Cheyne-Stokes Respirations (CSR)

Cheyne-Stokes respirations (CSR) are a form of periodic breathing characterized by cyclical fluctuations in respiratory depth and rate. This pattern consists of a crescendo-decrescendo sequence of hyperpnea followed by apnea, typically over a 30–120 second cycle.
Pathophysiology
CSR results from delayed feedback in the respiratory control system, often due to:
Prolonged circulation time (e.g., in heart failure)
Neurologic impairment (e.g., brainstem dysfunction)
Metabolic encephalopathy
Increased sensitivity to CO₂ and impaired cerebrovascular autoregulation may contribute. The brainstem chemoreceptors overcorrect in response to arterial gas changes, causing oscillations in ventilation.
Etiologies
1. Neurologic Causes
Increased Intracranial Pressure (ICP): Often the earliest abnormal respiratory pattern observed.
Seen with traumatic brain injury, brain tumors, cerebral hemorrhage, or stroke.
Associated signs: ↓ LOC, pupillary changes, Cushing’s triad (hypertension, bradycardia, irregular respirations).
Hypertensive Encephalopathy:
Sudden onset CSR with altered mental status, seizures, papilledema, vision changes.
Severe hypertension precedes symptoms.
Brainstem Lesions:
Direct compression or ischemia to the pons or medulla.
May signal impending herniation.
2. Cardiopulmonary Causes
Congestive Heart Failure (CHF):
Particularly in left-sided heart failure, where circulation time is prolonged.
Accompanied by exertional dyspnea, orthopnea, fatigue, tachycardia, and pulmonary congestion (crackles).
Often occurs during sleep.
Pulmonary Edema or Hypoxemia:
May trigger periodic breathing in the context of impaired gas exchange.
3. Renal Failure
End-stage renal disease (ESRD):
Uremic encephalopathy may manifest with CSR.
Associated signs: oral ulcers, ammonia breath, coagulopathy, mental status changes.
4. Drug-Induced
CNS depressants (e.g., opioids, benzodiazepines, barbiturates):
Suppression of medullary respiratory centers can provoke periodic breathing.
Evaluate for overdose or polypharmacy, especially in geriatric or palliative settings.
5. Physiologic or Non-Pathologic
High-altitude adaptation:
Common in individuals newly exposed to high elevations (>2,500 m).
Elderly during sleep:
May be observed in otherwise healthy older adults during NREM sleep stages.
Table: Causes of Cheyne-Stokes Respirations
Cause | Pathophysiology | Key Clinical Features |
Left-Sided Heart Failure | Prolonged circulation time delays feedback to respiratory center | Exertional dyspnea, orthopnea, fatigue, tachypnea, tachycardia, pulmonary crackles, nonproductive or blood-tinged cough |
Hypertensive Encephalopathy | Severe hypertension leads to cerebral edema and impaired autoregulation | Headache, seizures, vomiting, papilledema, decreased LOC, vision changes (blurring, transient blindness), transient paralysis |
Increased Intracranial Pressure (ICP) | Brainstem dysfunction disrupts respiratory center control | Early: altered LOC, headache, vomiting, unequal pupils, blurred vision; Late: bradycardia, widened pulse pressure, abnormal posturing |
Chronic Renal Failure (Uremia) | Toxin accumulation affects CNS function | Bleeding gums, uremic fetor (ammonia breath), oral ulcers, fatigue, altered LOC, pericardial rub, fluid overload |
Traumatic Brain Injury | Cerebral edema and pressure on brainstem | LOC changes, seizures, vomiting, focal neurological deficits, signs of cerebral herniation |
Stroke (especially brainstem) | Damage to medullary respiratory centers | Sudden onset hemiplegia, dysphagia, altered consciousness, pupillary abnormalities, cranial nerve deficits |
Drug Overdose (e.g., opioids, barbiturates, benzodiazepines) | CNS depression affects respiratory drive | Miosis, bradypnea/apnea, decreased LOC, hypoventilation, hypotension |
Carbon Monoxide Poisoning | Hypoxic injury to the brain affects respiratory regulation | Headache, confusion, cherry-red skin (rare), nausea, vomiting, altered mental status, seizures |
High Altitude Exposure | Hypoxia triggers unstable respiratory control during sleep | Seen in unacclimatized individuals; may cause periodic breathing, dizziness, fatigue, insomnia, and sleep disturbances |
Central Sleep Apnea | Intermittent loss of respiratory effort during sleep due to CNS dysfunction | Snoring, daytime sleepiness, witnessed apnea, poor sleep quality; often associated with heart failure and neurologic conditions |
Brain Tumors | Compression or infiltration of brainstem | Progressive neurological symptoms, morning headaches, vomiting, vision changes, altered mental status |
Meningitis/Encephalitis | Inflammation or infection of the brain affecting respiratory centers | Fever, neck stiffness, altered LOC, photophobia, seizures, vomiting, focal neurological signs |
Sepsis (Late Stage) | Multiorgan failure and metabolic encephalopathy | Tachypnea, hypotension, fever or hypothermia, confusion, poor perfusion, organ dysfunction |
Clinical evaluation
Initial assessment
Vital signs: Monitor for bradycardia, widened pulse pressure (late ICP sign), hypoxia.
Airway management: Ensure patency; apply supplemental O₂.
Neurologic exam:
Assess Glasgow Coma Scale (GCS).
Evaluate pupils for size, symmetry, and reactivity.
Observe for motor deficits or posturing.
Respiratory monitoring
Observe respiratory cycles for 3–4 minutes to characterize the pattern.
Time and document:
Duration of hyperpnea
Duration of apnea
Oxygen desaturation trends
Monitor for prolonged apneic events and associated desaturation or cyanosis.
Emergency interventions
In suspected neurologic injury
Elevate head of bed to 30 degrees to reduce ICP.
Rapidly obtain baseline neurologic status.
Frequently reassess LOC, motor function, and pupillary responses.
Initiate ICP monitoring if indicated.
Prepare for endotracheal intubation if respiratory effort deteriorates.
Investigations
Test | Purpose |
ABG | Evaluate hypoxia, hypercapnia, and acid-base status |
CT/MRI Brain | Assess for mass effect, infarct, or hemorrhage |
EEG | In encephalopathic patients or if seizure activity is suspected |
ECG & Echo | Assess for CHF or ischemia |
BUN, Creatinine | Identify uremia as a contributing factor |
Toxicology screen | Evaluate for CNS depressants or drug overdose |
Sleep Study (Polysomnography) | In chronic CSR suspected from CHF or central sleep apnea |
Differentiation from Other Patterns
Pattern | Features |
Cheyne-Stokes | Gradual crescendo-decrescendo followed by apnea |
Central Sleep Apnea | Sudden cessation of breathing without effort |
Obstructive Sleep Apnea | Apnea with ongoing respiratory effort and airway collapse |
Biot’s (Ataxic) Breathing | Irregular rhythm and depth with unpredictable apneas (often terminal) |
Kussmaul’s Respiration | Deep, rapid breathing due to metabolic acidosis |
Treatment & management
Address underlying cause
CHF: Optimize heart failure management (ACE inhibitors, diuretics, beta-blockers, consider adaptive servo-ventilation in CSA).
ICP Elevation: Neurosurgical intervention, hyperosmolar therapy (mannitol, hypertonic saline), ICP monitoring.
Toxic/metabolic causes: Dialysis for uremia, reversal agents for drug toxicity (e.g., naloxone).
Supportive measures
Administer oxygen cautiously; avoid suppressing respiratory drive in hypercapnic patients.
Consider positive airway pressure therapy (CPAP, BiPAP, ASV) in central sleep apnea.
Ensure adequate nutrition and hydration in chronically ill patients.
Special populations
Pediatrics
CSR is rare in children and typically associated with terminal heart failure or severe neurologic injury.
Geriatrics
May be a normal sleep-related pattern in elderly, particularly during Stage I or II NREM sleep.
Differentiate from sleep apnea and assess in the context of overall neurologic and cardiac function.
Patient & family education
Educate caregivers about differences between sleep apnea and CSR.
Discuss warning signs that indicate emergency deterioration (altered LOC, seizure, abnormal pupils).
In chronic cases, involve pulmonary or sleep medicine specialists for long-term management (e.g., central sleep apnea in CHF).
References
D’Elia E, Vanoli E, La Rovere MT, et al. Adaptive servo ventilation reduces central sleep apnea in chronic heart failure patients. J Cardiovasc Med. 2012;14(4):296–300.
Randerath WJ, Nothofer G, Priegnitz C, et al. Long-term auto servo-ventilation or constant positive pressure in heart failure and co-existing central with obstructive sleep apnea. Chest. 2013;143(6):1833.
D’Elia E, Vanoli E, La Rovere MT, Fanfulla F, Maggioni A, Casali V, Mortara A. Adaptive servo ventilation reduces central sleep apnea in chronic heart failure patients: beneficial effects on autonomic modulation of heart rate. J Cardiovasc Med. 2012;14(4):296–300.
Randerath WJ, Nothofer G, Priegnitz C, Anduleit N, Treml M, Kehl V, Galetke W. Long-term auto servo-ventilation or constant positive pressure in heart failure and co-existing central with obstructive sleep apnea. Chest. 2012;143(6):1833–41.
Parshall MB, Schwartzstein RM, Adams L, Banzett RB, Manning HL, Bourbeau J, et al. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med. 2012;185(4):435–52.
Naughton MT. Pathophysiology and treatment of Cheyne-Stokes respiration. Curr Opin Pulm Med. 2012;18(6):550–5.
Brack T, Thüer I, Clarenbach CF, Senn O, Russi EW, Bloch KE. Daytime Cheyne-Stokes respiration in chronic heart failure. Am J Respir Crit Care Med. 2007;176(8):813–8.
Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med. 1996;335(14):949–54.
Somers VK, White DP, Amin R, Abraham WT, Costa F, Culebras A, et al. Sleep apnea and cardiovascular disease: an American Heart Association/American College of Cardiology Foundation Scientific Statement. Circulation. 2008;118(10):1080–111.
Ropper AH, Samuels MA, Klein JP. Adams and Victor’s Principles of Neurology. 11th ed. New York: McGraw-Hill Education; 2019.
Guyton AC, Hall JE. Textbook of Medical Physiology. 14th ed. Philadelphia: Elsevier; 2020.
Kushida CA, editor. Encyclopedia of Sleep. 2nd ed. San Diego: Academic Press; 2019.