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Cheyne stokes

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"Cheyne-Stokes respiration"[MeSH Terms]

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Cheyne-Stokes Respiration

Definition and Pattern

Cheyne-Stokes respiration (CSR) is a pattern of periodic breathing characterized by rhythmic, cyclical alternation between hyperpnea and apnea. The hallmark is a smooth crescendo-decrescendo (waxing and waning) change in tidal volume, which peaks and then tapers down to a central apnea lasting typically 15-60 seconds, after which the cycle repeats.
  • Apneic phase: 15-60 seconds; arterial CO2 is at its lowest at apnea onset
  • Hyperpneic phase: usually lasts longer than the apneic phase
  • CO2 tension varies by ~14 mmHg and SpO2 by up to 18% across each cycle
The pattern was first graphically described by William Stokes (1854), based on an earlier account by John Cheyne.
Abnormal respiratory patterns and corresponding brain lesion levels - Cheyne-Stokes (A) is the waxing/waning trace at the top

Pathophysiology / Mechanism

CSR arises from instability in the respiratory control loop, not depression of it. The respiratory response to CO2 is actually heightened (not blunted) in CSR.
Two main mechanisms operate:

1. Prolonged Lung-to-Brain Circulation Time (main mechanism in heart failure)

  • In heart failure, slowed circulation means pulmonary capillary blood gases reach the medullary chemoreceptors with an abnormal delay - roughly 180 degrees out of phase with current alveolar gas tensions.
  • Hyperventilation lowers alveolar CO2, but before this low-CO2 blood reaches the brain, more low-CO2 blood has accumulated. When it finally arrives, the brain sees a sudden fall in CO2, suppresses breathing (apnea), then the cycle resets.
  • The feedback loop is too long - it oscillates.

2. Enhanced CO2 Chemosensitivity (neurologic/general)

  • Patients with increased chemosensitivity overrespond to CO2: small rises drive marked hyperventilation, which overshoots, driving CO2 below the apnea threshold.
  • Neural reflexes from extravascular lung fluid and elevated left atrial pressure further amplify the ventilatory drive.
  • During waking, descending cortical pathways prevent post-hyperventilation apnea. During sleep or forebrain impairment, this "damping" is removed and oscillations emerge.
(Plum and Posner's Diagnosis and Treatment of Stupor and Coma; Ganong's Review of Medical Physiology; Fishman's Pulmonary Diseases and Disorders)

Causes and Associations

CategoryExamples
CardiacCongestive heart failure (most common - occurs in 20-40% of LV systolic dysfunction)
NeurologicMetabolic encephalopathy (uremia, hepatic failure), bilateral forebrain or diencephalic lesions, cerebral infarcts, forebrain mass with diencephalic shift, pontine tegmentum lesions
PhysiologicNormal infants, healthy elderly, high altitude
Drugs/toxinsRespiratory depressants (e.g., morphine), raised intracranial pressure
SleepPredominantly NREM sleep; resolves in REM sleep
Risk factors in heart failure: male sex, advanced age, low baseline PaCO2, atrial fibrillation.
CSR represents about 5-10% of all sleep apnea cases and is uncommon outside heart failure.

Neurological Localization

CSR is classically associated with lesions at the forebrain/diencephalic level (see panel A in the figure above). As lesions descend:
  • Pons: apneustic breathing (inspiratory pauses)
  • Pontomedullary junction: cluster/ataxic breathing
  • Ventrolateral medulla: apnea
This makes CSR a useful localizing sign in comatose patients - it implies the brainstem itself is intact, with supratentorial or diencephalic dysfunction.
(Plum and Posner's; Localization in Clinical Neurology; Bradley and Daroff's Neurology in Clinical Practice)

Clinical Features and Diagnosis

  • Patients may report fatigue, daytime sleepiness, and paroxysmal nocturnal dyspnea (PND - a classic heart failure symptom, often caused by underlying CSR)
  • Arousals occur during the hyperpneic phase (unlike OSA where arousals correlate with airflow obstruction)
  • Bedside diagnosis: careful observation of breathing pattern; crescendo-decrescendo respirations visible
  • Sleep lab (PSG): gold standard; CSR resolves in REM sleep; arousals on EEG during hyperpnea
  • CSR does not resolve immediately with CPAP (distinguishing it from OSA)
  • Mental status fluctuations and EEG changes may occur due to swings in cerebral blood flow

Treatment

  1. Treat the underlying cause first - optimizing heart failure management (diuretics, ACE inhibitors, beta-blockers, etc.) often resolves CSR
  2. CPAP: improves breathing indices but not superior to optimal medical therapy for mortality; does not work immediately
  3. Adaptive servo-ventilation (ASV): improves CSR and quality of life but the SERVE-HF trial showed increased mortality in heart failure with reduced EF - avoid ASV in HFrEF
  4. Transvenous phrenic nerve stimulation (remedē System): FDA-approved implantable device; normalizes central apnea indices and improves SpO2, but mortality data still pending
  5. Supplemental O2: can reduce hypoxic oscillations
  6. Theophylline (respiratory stimulant): occasionally used but limited evidence
(Goldman-Cecil Medicine; Murray & Nadel's Respiratory Medicine)

Key Distinguishing Points: CSR vs. OSA

FeatureCSROSA
PatternSmooth crescendo-decrescendoAbsent airflow with effort
ArousalsDuring hyperpneic phaseEnd of apnea
REM sleepResolvesPersists or worsens
Response to CPAPGradual, incompleteImmediate
TypeCentral apneaObstructive apnea
Sources: Plum and Posner's Diagnosis and Treatment of Stupor and Coma; Goldman-Cecil Medicine; Fishman's Pulmonary Diseases and Disorders; Ganong's Review of Medical Physiology, 26th ed.; Murray & Nadel's Textbook of Respiratory Medicine; Localization in Clinical Neurology, 8e.
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