Cheyne-Stokes respiration in heart failure: friend or foe? Hemodynamic effects of hyperventilation in heart failure patients and healthy volunteers

In patients with heart failure (HF), Cheyne-Stokes respiration (CSR) is characterized by chronic hyperventilation (HV) with low arterial partial pressure of carbon dioxide (pCO(2)). It is still unclear whether this HV represents a compensatory response to HF or an independent comorbidity. This study investigated the hemodynamic effects of HV in HF patients and volunteers. A total of 15 volunteers [13 male, 25 +/- A 4 years, brain natriuretic peptide (BNP) < 49 pg/mL, left ventricular rejection fraction (LVEF) > 55 %) and 20 HF patients with reduced LVEF (15 male, 67.7 +/- A 12 years, NYHA class 2.6 +/- A 0.6, BNP 790 +/- A 818 pg/mL, LVEF 32.4 +/- A 7.3 %) were enrolled. Hemodynamics was monitored noninvasively in volunteers (TaskForce Monitor, CNSystems) and invasively in HF patients. During HV, the transcutaneous CO2 pressure in volunteers decreased from 38.7 +/- A 2.5 to 28.6 +/- A 3.3 mmHg (p < 0.001) and pCO(2) in HF patients decreased from 33.6 +/- A 3.7 to 22.2 +/- A 3.2 mmHg (p < 0.001). There was a significant increase in cardiac output (CO) in both volunteers (6.2 +/- A 1.3-7.5 +/- A 1.3 L/min, p < 0.001) and HF patients (4.4 +/- A 1.3-5.0 +/- A 1.3 L/min), mainly as a result of an increase in heart rate (67.4 +/- A 7.6-82.8 +/- A 10.9/min, p < 0.001; and 77.2 +/- A 17.7-86.2 +/- A 22.4/min, p < 0.001, respectively); stroke volume (SV) was unchanged in volunteers (93.7 +/- A 19.6-93.8 +/- A 21.4 mL) and only slightly increased in HF patients (64.4 +/- A 28.7-68.5 +/- A 23.2 mL). CSR with associated HV may be a compensatory mechanism in patients with a failing heart. This compensatory mechanism includes an increase in heart rate, which might be deleterious in the long run.