High-Flow-Therapy for the Treatment of Cheyne-Stokes-Respiration in Chronic Heart Failure

In chronic heart failure (CHF) patients sleep disordered breathing mainly comprises two different entities: obstructive sleep apnea (OSA) and central sleep apnea with Cheyne-Stokes respiration (CSA). Being a rare disease in the general population, CSA is found with a prevalence of up to 40% in CHF patients.1 This rise in prevalence is instigated by pathophysiological overlapses. CSA is precipitated by hyperventilation and a highly sensitive hypocapnea-induced apneic threshold, whereby apnea is then initiated by small transient reductions in partial pressure of carbon dioxide (pCO2). Underlying mechanisms are not fully understood, yet. Despite neurohumoral derangement such as altered chemoreflex cascades (enhanced "loop gain" and "controller gain") and circulatory delay, pulmonary congestion is thought to play a role in the evolution of CSA. Caused by reduced cardiac output and/or impaired left ventricular filling pattern, a rise in pulmonary capillary wedge pressure (PCWP) with resulting interstitial pulmonary edema is closely correlated to the occurrence of CSA. Furthermore, acute increase in pulmonary congestion by overnight rostral fluid displacement to the lungs was found to lower sleep pCO2 and predisposed to CSA. Furthermore, decreased blood oxygen tension stimulates the discharge of peripheral chemoreceptors and gives rise to hyperventilation pattern of CSA. Conversely, hyperventilation increases the propensity for central apneas by reducing the CO2-reserve. Underlining the importance of hypoxemic chemoreceptor stimulation in the development of CSA, previous studies exemplified this as a pathophysiological key element in patient with pulmonary artery hypertension, where hypocapnia, periodic breathing and CSA is highly prevalent despite normal capillary wedge pressure values. Also in heart failure patients this seems to be important: several interventional studies showed an at least partial suppression of CSR using oxygen therapy.

High flow therapy is a technique that provides a range of flows of heated, humidified air to patients requiring respiratory support, delivered through nasal cannula range The high flow ventilation therapy with an air/oxygen mixture at a rate of 20-50 L/min via a nasal cannula is able to provide adequate oxygen flow rates to completely avoid hypoxemias. An increase in oxygen saturation is associated with a reduced chemosensitivity of the glomus caroticum. This may further help to improve Cheyne-Stokes respiration severity. Previous studies could reach a reduction of 50% of the AHI with the use of 2 L/min of oxygen.

At the same time the high flow ventilation therapy can attenuate inspiratory resistance by potentially delivering positive distending pressure for lung recruitment without providing excessive intrathoracic pressure (only 3-6 cm H2O, according to manufacturer).

But on the other hand the hyperoxemic state was also found to have some unfavorable consequences such as an increase in infarct size after myocardial infarction and should therefore be avoided.

The FLOAT-CS study is a proof-of-concept study that investigates nocturnal high flow ventilation therapy with oxygen (oxygen-HFT) as a novel therapeutic approach for HFrEF patients with CSA by attenuation of the hypoxemic burden.