Fluctuations in End-Expiratory Lung Volume during Cheyne-Stokes Respiration

Abstract

We hypothesized that patients with Cheyne-Stokes respiration exhibit periodic increases in end-expiratory lung volume, mediated by changes in breath components, postinspiratory inspiratory muscle activity, or both. Calibrated inductive plethysmography revealed that 12 of 12 patients with Cheyne-Stokes respiration experienced increases in end-expiratory volume during hyperpnea: maximum 412 +/- 112 (SE) ml (range 75-1,543 ml). Compared with quiet breathing, the breath with largest increase in end-expiratory volume had larger tidal volume (867 +/- 107 vs. 567 +/- 38 ml, p < 0.01) and shorter expiratory time (1.25 +/- 0.11 vs. 1.66 +/- 0.15 seconds, p < 0.05). During decrescendo, the breath with largest decrease in end-expiratory volume had smaller tidal volume (p < 0.01) and longer expiratory time (p < 0.01). Cross-correlation of time series revealed that end-expiratory volume was related to both breath components (p < 0.0001). Bipolar needle electrodes revealed that scalene muscle activity at end-expiration was 50.7 +/- 14.0% higher at highest increase in lung volume than during preceding apnea (p < 0.05). Time series for scalene activity and end-expiratory volume were cross-correlated (p < 0.008). Increase in tonic scalene activity at end-expiration, however, was equivalent during crescendo and decrescendo phases: 50.6 +/- 22.1 versus 42.0 +/- 12.9% (p = 0.48). In conclusion, patients with Cheyne-Stokes respiration exhibit fluctuations in end-expiratory lung volume, primarily because of alterations in tidal volume and expiratory time rather than postinspiratory inspiratory muscle activity.

Distinct Patterns of Hyperpnea During Cheyne-Stokes Respiration: Implication for Cardiac Function in Patients With Heart Failure

“…35 However, in that study periodic breathing was examined during wakefulness both while breathing spontaneously and during hypoxic gas inhalation. For this reason, those results may not be comparable to ours.…”

Cheyne–Stokes respiration: friend or foe?: Figure 1

“…First, end-expiratory lung volume increases by 0.1–1.5 l (mean 400 ml) with the cyclic hyperventilation of CSA–CSR (see figure 1A). 23 Increased lung volume would increase oxygen stores, offset the restrictive ventilatory defect and impaired transfer factor of the lung for carbon monoxide commonly observed in advanced HF,3 thus increasing peripheral oxygen saturation, reducing loop gain and resulting in reduced severity of CSA–CSR 24. The increase in end-expiratory lung volume that occurs periodically with CSA–CSR is similar to the effects observed constantly with CPAP of approximately 500 ml 25…”

Cheyne-Stokes Respiration in Patients with Heart Failure: Prevalence, Causes, Consequences and Treatments

“…CPAP increases intrathoracic pressure, which decreases both afterload by lowering transmural cardiac pressure and preload by lowering the venous return, so that cardiac function improves in patients with high ventricular filling pressures [95,96,97]. Additionally, CPAP may interrupt CSR by counteracting the periodic oscillations of the end-expiratory lung volume during CSR [98]. In a randomized trial with 66 patients over 5 years, CPAP improved LVEF by 7% and decreased the combined rate of mortality and transplantation in the group of 29 patients with CSR while the 37 patients without CSR did not benefit from CPAP [44].…”