Cheyne Stokes respiration is an abnormal breathing pattern

Checking your browser before accessing www.ncbi.nlm.nih.gov · Click here if you are not automatically redirected after 5 seconds

This can be clinically observed and documented with a cyclic variation of breathing pattern with a change in saturation from 90% to 100%. Minute ventilation is not routinely monitored during sleep studies. The hyperventilation is documented by rising and falling chest excursions and the tidal ...

Cheyne-Stokes respiration is an abnormal breathing pattern which commonly occurs in patients with decompensated congestive heart failure and neurologic diseases, in whom periods of tachypnea and hyperpnea alternate with periods of apnea. In the ...

Cheyne–Stokes respiration (CSR) is a form of periodic breathing characterized by apneas or hypopneas interposed by a characteristic breathing pattern that begins almost imperceptibly, waxes until a peak ventilation, and then wanes until the next respiratory event (i.e., apnea or hypopnea) ...

Patients with CHF may present both central and obstructive sleep apnea,7, 8, 9, 10, 11, 12, 13, 14, 15 may convert obstructive to central sleep apnea during a single night,16 and may present obstructive apneas with a prolonged ventilatory pattern that mimics Cheyne-Stokes respiration.17 In this text for the sake of simplicity, unless otherwise stated, Cheyne-Stokes respiration will imply that it is associated with central apnea (Fig. 1). ... Figure 1. Polysomnographic recordings of a congestive heart failure presenting Cheyne-Stokes respiration during sleep. The top channels are related to sleep recordings. The bottom channels trac respiration by monitoring motion of the thorax, abdomen and respiratory flow (nasal canula). Observe the typical crescendo-decrescendo tidal volume interposed with central apneas

However, Hoffman and associates, studying patients with cardiogenic pulmonary edema, found no differences in left ventricular ejection fractions in patients with or without Cheyne–Stokes breathing.89 Hall and colleagues found that circulatory delay did correlate with Cheyne–Stokes cycle length, but not with apnea length.90 Lorenzi-Filho and co-workers showed that CO2 inhalation blocked Cheyne–Stokes breathing in patients with heart failure and argued that reduction in Paco2 sensed by peripheral chemoreceptors triggered central apneas.88 The issue of an abnormal feedback to the CNS in the genesis of respiratory oscillations was studied in animals by Cherniack91 who used the normal phrenic nerve stimulus to trigger a mechanical ventilator that had been modified so that the gain could be varied to amplify or retard the induced tidal volume triggered by the phrenic stimulus.

This can be clinically observed and documented with a cyclic variation of breathing pattern with a change in saturation from 90% to 100%. Minute ventilation is not routinely monitored during sleep studies. The hyperventilation is documented by rising and falling chest excursions and the tidal ...

This certainly describes control of normal respiration, but to produce an unstable state such as C-SR requires either a very long transit time (3½ min) or an increase of the controller gain (13 times), physiologically improbable. There is general agreement that apnea initiates C-SR but that has not been well explained except for post-hyperventilation apnea, and that explanation is not compatible with a study by Nielsen and Smith in 1951.