Hypercapnia Attenuates Ventricular Ectopy during Wakefulness in a Young Man with Heart Failure

Ventricular premature beats (VPBs) are common in heart failure (HF). Patients with HF often exhibit oscillations in breathing pattern (or Cheyne‐Stokes Respiration, CSR) that lead to increased VPBs during the hyperpneic phase. In such patients, CO 2 inhalation during sleep eliminates CSR and reduces VPB prevalence. Whether this VPB‐lowering effect of CO 2 occurs in awake HF patients without CSR remains unexplored. In a young CSR‐free HF patient (26 years; LVEF=20%; BMI=30 kg·m −2 ) with mild obstructive sleep apnea (AHI=17 events/h) and frequent ectopy, we compared the incidence of VPBs during: 1) resting breathing; 2) volitional hyperventilation; 3) and at standardized intervals (quartiles) during two CO 2 rebreathing tests with end‐tidal O 2 tension (P ET O 2 ) maintained at either 50 mmHg (hypercapnic‐hypoxia) or 150 mmHg (hypercapnic‐hyperoxia). Breath‐by‐breath ventilation, P ET O 2 , and P ET CO 2 were measured by flowmeter and rapid gas analyzer and ECG and O 2 saturation were monitored continuously. At rest (P ET CO 2 =39 mmHg) and during hyperventilation (P ET CO 2 =28 mmHg), VPBs occurred with 15% and 12% of all heart beats, respectively. With hyperoxic CO 2 rebreathing (P ET O 2 =148mmHg), as P ET CO 2 increased from 40, 46, 52, 57 mmHg in the first through fourth quartile, VPB incidence decreased from 11% to 6%, 3%, and 0%, respectively. Hypoxic rebreathing (P ET O 2 =51mmHg) showed a similar trend: VPB incidence fell from 9% at a P ET CO 2 of 40 mmHg to 0% at 46 mmHg and remained at 0% thereafter. The hypercapnia‐induced reduction in VPB frequency was not dependent on heightened ventilation: VPBs were evident during volitional hyperventilation (12%) but not during the CO 2 rebreathing quartiles with matched ventilation (0% for both hypoxia and hyperoxia). Furthermore, blood O 2 also did not appear to modulate this response: VPB incidence at rest (15%) was similar to both hypoxic (11%; O 2 saturation=86%) and hyperoxic (13%; O 2 saturation=99%) CO 2 rebreathing quartiles with matched ventilation (~9 L·min −1 ) and P ET CO 2 (~39 mmHg). These observations suggest that in HF, acute hypercapnia attenuates ventricular ectopy. The mechanism appears to be unrelated to increased respiratory or sympathetic drive, myocardial stretch accompanying large tidal volumes, or altered O 2 availability. How hypercapnia exerts anti‐arrhythmic effects remain uncertain; we hypothesize that CO 2 mediated increases in coronary flow may be involved. Support or Funding Information Experiments were funded by a Project Grant from the Canadian Institutes of Health Research (PJT 159491).

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