From the Guidelines
Cheyne-Stokes respiration is primarily caused by delayed feedback in the respiratory control system, often due to prolonged circulation time between the lungs and brain, commonly occurring in patients with severe heart failure. The etiology of Cheyne-Stokes respiration can be attributed to various factors, including neurological conditions, metabolic disturbances, and high-altitude exposure. According to the study by RB Berry et al. 1, Cheyne-Stokes breathing is a specific form of periodic breathing characterized by a crescendo-decrescendo pattern of respiration between central apneas or central hypopneas. This pattern is often associated with unrecognized congestive heart failure and is a risk factor for early mortality or the need for heart transplant in patients with known heart failure.
Key Factors Contributing to Cheyne-Stokes Respiration
- Delayed feedback in the respiratory control system
- Prolonged circulation time between the lungs and brain
- Severe heart failure
- Neurological conditions such as strokes, brain tumors, traumatic brain injuries, and increased intracranial pressure
- Metabolic disturbances like uremia in kidney failure
- High-altitude exposure
The study by W H A T I S C SA - H C S B? 1 suggests that the prevailing hyperventilation and secondary low PaCO2 that characterize Cheyne-Stokes respiration are thought to be caused by at least four potential mechanisms, including pulmonary venous congestion, increased sympathetic activity, loss of endothelial nitric oxide activity in the carotid bodies, and increased physiological pulmonary dead space in patients with heart failure. The primary mechanism involves an unstable feedback loop in the respiratory control system, where the brain overcompensates for changes in blood oxygen and carbon dioxide levels, leading to oscillations in breathing effort. This underlying mechanism is supported by the study by RB Berry et al. 1, which highlights the importance of recognizing Cheyne-Stokes respiration as a risk factor for early mortality or the need for heart transplant in patients with known heart failure.
From the Research
Etiology of Cheyne-Stokes Respiration
The etiology of Cheyne-Stokes respiration is complex and multifactorial. Some of the key factors that contribute to its development include:
- Severe congestive heart failure, which is considered the most important risk factor for the development of Cheyne-Stokes respiration 2
- Increased CNS sensitivity to changes in arterial PCO2 and PO2, resulting in increased central controller gain 3
- Decrease in total body stores of CO2 and O2, leading to instability in arterial blood gas tensions in response to changes in ventilation (underdamping) 3
- Increased circulatory time 3
- Hyperventilation-induced hypocapnia, which seems to be an important determinant for the development of Cheyne-Stokes respiration 3
- Sleep disruption, arousals, hypoxemia-reoxygenation, hypercapnia/hypocapnia, and changes in intrathoracic pressure, which have harmful effects on the cardiovascular system 2
Pathophysiology
The pathophysiology of Cheyne-Stokes respiration involves the cardiovascular, pulmonary, and sympathetic nervous systems 4. It is characterized by a crescendo-decrescendo pattern of respiration, which is a compensation for the changing levels of blood oxygen and carbon dioxide 2. The cyclic oscillations of tidal volume and respiratory rate with periods of hyperpnea alternating with hypopnea or apnea can harm the failing heart through intermittent hypoxia and recurrent sympathetic surges 5.
Clinical Implications
Cheyne-Stokes respiration is associated with increased mortality and morbidity in patients with heart failure 2, 3, 6. It impairs the quality of life and increases cardiac mortality in patients with heart failure 5. Therefore, it is essential to actively pursue Cheyne-Stokes respiration in patients with severe heart failure and provide prompt diagnosis and treatment 6.