Apnea–Hypopnea Threshold for CO₂ in Patients with Congestive Heart Failure

Abstract

To understand the pathogenesis of central sleep apnea (CSA) in patients with congestive heart failure (CHF), we measured the end-tidal carbon dioxide pressure (PET(CO2)) during spontaneous breathing, the apnea-hypopnea threshold for CO2, and then calculated the difference between these two measurements in 19 stable patients with CHF with (12 patients) or without (7 patients) CSA during non-rapid eye movement sleep. Pressure support ventilation was used to reduce the PET(CO2) and thereby determine the thresholds. In patients with CSA, 1.5-3% CO2 was supplied temporarily to stabilize breathing before determining the thresholds. Unlike patients without CSA whose eupneic PET(CO2) increased during sleep (37.7 +/- 1.4 mm Hg versus 40.2 +/- 1.5 mm Hg, p < 0.01), patients with CSA showed no rise in PET(CO2) from wakefulness to sleep (37.5 +/- 0.9 mm Hg versus 38.2 +/- 1.0 mm Hg, p = 0.2). Patients with CHF and CSA had their eupneic PET(CO2) closer to the threshold PET(CO2) than patients without CSA (DeltaPET(CO2) [eupneic PET(CO2) - threshold PET(CO2)] was 2.8 +/- 0.3 mm Hg versus 5.1 +/- 0.7 mm Hg for apnea, p < 0.01; 1.7 +/- 0.7 versus 4.1 +/- 0.5 mm Hg for hypopnea, p < 0.05). In summary, patients with CHF and CSA neither increase their eupneic PET(CO2) during sleep nor proportionally decrease their apnea-hypopnea threshold. The resultant narrowed DeltaPET(CO2) predisposes the patient to the development of apnea and subsequent breathing instability.

Sleep Apnea and Cardiovascular Disease

“…354 Diuresis with a reduction in cardiac filling pressure also has been shown to reduce the severity of CSA, 340 but in some patients, the resulting metabolic alkalosis may promote CSA by narrowing the difference between ambient PaCO 2 and the PaCO 2 threshold for apnea. 355,356 ␤-Adrenergic blockade, which counters excess sympathetic activation and may modulate ventilatory responses in heart failure, 18 has been reported to decrease AHI in patients with CSA. 357 However, the increasing use of such antagonists in heart failure appears not to have altered the prevalence of CSA in this condition.…”

Sleep disordered breathing in patients with heart failure

“…On the other hand hypocapnia in HF subjects with impaired ejection fraction (mean EF 23%) was associated with increased number of AHI episodes and central apneas [30]. Thus, it may not be hypocapnia itself, but diminished difference between eupneic PCO 2 and apnea threshold, known as PCO 2 reserve that predisposes to CSA, as discussed earlier [24,25].…”

“…Pathological mechanisms underlying CSA have been widely investigated within last decade and explained in detail in a recent monograph [24]. The important factors involved in pathophysiology of CSA are: diminished PCO 2 reserve (difference between eupneic PCO 2 and apnea threshold) [24, 25], and augmented central and peripheral hypoxic and hypercapnic chemosensitivity [26,27]. These will be discussed in details below (Fig.…”

End-Tidal CO₂ Tension Is Predictive of Effective Nocturnal Oxygen Therapy in Patients with Chronic Heart Failure and Central Sleep Apnea

“…It was reported that CHF patients with CSA showed no rise in P ET CO 2 from wakefulness to sleep unlike patients without CSA whose P ET CO 2 increases during sleep (Xie et al 2002). This means the narrowed proximity of the eupneic PaCO 2 to the apnea threshold, which may be a crucial determinant of the susceptibility to apnea.…”