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

OBJECTIVE

In patients with heart failure (HF), Cheyne-Stokes respiration (CSR) is characterized by chronic hyperventilation (HV) with low arterial partial pressure of carbon dioxide (pCO2). 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.

METHODS

A total of 15 volunteers [13 male, 25 ± 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 ± 12 years, NYHA class 2.6 ± 0.6, BNP 790 ± 818 pg/mL, LVEF 32.4 ± 7.3 %) were enrolled. Hemodynamics was monitored noninvasively in volunteers (TaskForce Monitor, CNSystems) and invasively in HF patients.

RESULTS

During HV, the transcutaneous CO2 pressure in volunteers decreased from 38.7 ± 2.5 to 28.6 ± 3.3 mmHg (p < 0.001) and pCO2 in HF patients decreased from 33.6 ± 3.7 to 22.2 ± 3.2 mmHg (p < 0.001). There was a significant increase in cardiac output (CO) in both volunteers (6.2 ± 1.3-7.5 ± 1.3 L/min, p < 0.001) and HF patients (4.4 ± 1.3-5.0 ± 1.3 L/min), mainly as a result of an increase in heart rate (67.4 ± 7.6-82.8 ± 10.9/min, p < 0.001; and 77.2 ± 17.7-86.2 ± 22.4/min, p < 0.001, respectively); stroke volume (SV) was unchanged in volunteers (93.7 ± 19.6-93.8 ± 21.4 mL) and only slightly increased in HF patients (64.4 ± 28.7-68.5 ± 23.2 mL).

CONCLUSIONS

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.