THE MECHANISM OF CHEYNE-STOKES RESPIRATION*

Abstract

Nine patients with heart disease and Cheyne-Stokes respiration had continuous measurements of arterial O2 saturations, ventilation and end tidal CO2. Cardiac output, arterial CO2 tension, pH and lung to artery circulation time were also determined. The results consistently showed hypocapnea, rarely O2 unsaturation and a temporal phasic shift of 180[degree] between respiratory gas values and blood gas values. The period of the respiratory arrhythmias was twice the lung to artery circulation time. By analogy the respiratory control system was considered to be oscillatory because of the partial loss of damping factors and increase in the feedback delay time and possibly an increased gain of the respiratory center. When the theoretical response of a normal respiratory center to sinusordial variations in PCO2 was investigated, hypocapnea resulted since the apneic phase caused the response to become non-linear. The authors conclude from postmortem studies that neurological disease is coincidental rather than primary. Several factors related to circulatory insufficiency combine to produce the phenomena of Cheyne-Stokes respiration.