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ULY CLINIC

ULY CLINIC

25 Mei 2025, 10:49:13

Cheyne-Stokes Respirations (CSR)

Cheyne-Stokes Respirations (CSR)
Cheyne-Stokes Respirations (CSR)
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
  1. 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.

  2. 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.

  3. 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.

  4. 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.

  5. 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.

  6. Naughton MT. Pathophysiology and treatment of Cheyne-Stokes respiration. Curr Opin Pulm Med. 2012;18(6):550–5.

  7. 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.

  8. Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med. 1996;335(14):949–54.

  9. 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.

  10. Ropper AH, Samuels MA, Klein JP. Adams and Victor’s Principles of Neurology. 11th ed. New York: McGraw-Hill Education; 2019.

  11. Guyton AC, Hall JE. Textbook of Medical Physiology. 14th ed. Philadelphia: Elsevier; 2020.

  12. Kushida CA, editor. Encyclopedia of Sleep. 2nd ed. San Diego: Academic Press; 2019.

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