Congestive Heart Failure and Central Sleep Apnea

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

“…Several mechanisms can contribute to hyperventilation in HF: stimulation of pulmonary juxtacapillary receptors by pulmonary congestion, increased peripheral and central chemoresponsiveness, and arousals from sleep. [3][4][5] Moreover, the increased lung-to-chemoreceptor circulation delay, typical of HF as a result of decreased cardiac output (CO), may contribute to the ventilatory instability. [3][4][5] The duration of the hyperpnea and apnea-hyperpnea cycle are directly proportional to the lung-to-peripheral chemoreceptor circulation time and inversely proportional to SV and CO. 6 Consequently, durations of hyperpnea and apnea-hyperpnea cycles can be used as indices of SV and CO.…”

Assessment of erythrocyte deformability in an obese case of chronic thromboembolic pulmonary hypertension

“…In the second admission to treat CTEPH, overnight polysomnography was performed and the diagnosis of central sleep apnea syndrome (CSAS) was obtained. CSAS is frequently associated with heart failure [4]. Actually BNP was 474 pg/mL (normal range < 20 pg/mL).…”

Sleep apnea syndrome and heart failure—mechanisms and consequences

“…CSR-CSA appears when partial pressure of carbon dioxide (PCO 2 ) decreased below the apnea threshold caused by hyperventilation (38) due to either stimulation of pulmonary juxta capillary receptors by pulmonary congestion, increased peripheral and central chemo responsiveness, or arousals from sleep (37,39,40). Also, decreased cardiac output may generate ventilatory instability because of increased lung-to-chemoreceptor circulation delay, which is directly proportional with the duration of an apnea-hyperpnea cycle (37,39,40). Fluid retention may also have a significant impact in the pathogenesis of CSA due to stimulation of pulmonary irritant receptor, which can lead to hyperventilation and hypocapnia (41,42).…”