Cheyne-Stokes respiration pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Pathophysiology in Patients with CHF
The exact mechanisms responsible for the development of CSR are unknown. Among the more important factors are hyperventilation, and a prolonged circulatory time.
- Hyperventilation and resultant hypocapnia, is thought to occur in patients with CHF due to stimulation of pulmonary mechanoreceptors by interstitial edema.
- Patients with CHF and CSR have been found to have lower awake and sleep PaCO2 levels, and increased minute ventilation as compared to patients with CHF without CSR.
- In addition, the apnea threshold (the PaCO2 below which apnea occurs) also seems to be increased in patients with CHF and CSR.
- Furthermore, hypoxemia shifts the ventilatory response curve for CO2 up and to the left (higher ventilation at any given CO2). This reduces the stability of the ventilatory control system.
- Thus, hyperventilation reduces the PaCO2 below the apnea threshold, and as PaCO2 rises, an exaggerated ventilatory response causes the PaCO2 to fall below the apnea threshold, and a vicious cycle ensued.
- Prolonged circulatory time, as a marker of severity of CHF, is directly correlated to the duration of sleep spent in CSR, as well as the cycle length of each episode.
- This is due to an increase in the oscillation around a set point PaO2 and PaCO2. As circulatory time increases, the PaO2 and PaOC2 become more out of phase with the respiratory pattern set by the ventilatory control centers (carotid body and medulla).
- It also seems that patients with CHF have less ability to buffer changes in PaCO2, i.e. the system is underdamped. This results from the fact that CHF causes a decrease in FRC, which reduces total body stores of CO2 and O2. It has been shown that, as total body stores of CO2 decrease, the body is not able to buffer the transient changes in PaCO2 as well.
Pathophysiology in Patients with Stroke
There is a lot less data on the mechanisms of CSR in patients with CNS disease, than in patients with CHF. Some potential mechanisms include a delay in afferent, efferent neural transmission, delays in central processing of afferent signals, slowed brain blood flow, and altered chemoresponsiveness with a heightened ventilatory responsiveness.