Treatment-Emergent Central Apnea

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Treatment-Emergent Central Apnea occurs when a person that has no to minimal Central Apnea starts using a CPAP/APAP/BiLevel device and sees a marked increase in Central Apnea.


  1. Initial use of a CPAP/APAP/BiLevel Device
  2. Increase in Pressure Support (PS) or EPR (Expiratory Pressure Relief)/Flex on a CPAP/APAP/BiLevel Device
  3. Increase in pressure on a CPAP/APAP/BiLevel Device
  4. Anything that increases the efficiency of your breathing


A Primary driver for breathing is a high level of pCO2 in the arterial blood that is sensed by Chemoreceptors. This is sensed and a signal to breathe is initiated. It is not a low level of oxygen that provides a signal to breathe, it is a high level of CO2. How does this occur? Our CPAP/APAP/BiLevel Devices are designed to improve our breathing. One part of this is to improve the exchange of blood gasses. When too much CO2 is washed out no signal to breathe is delivered, thus a Treatment-Emergent Central Apnea. Keep in mind that we are dealing with people who have been suffering from poor breathing for years. Their bodies have adjusted to this environment, they are used to higher levels of CO2 in their blood so lowering the CO2 to more 'normal' levels passes through a threshold that fails to produce a breathe now signal.


  1. Continued use of a CPAP/APAP/BiLevel Device. Treatment-Emergent Central Apnea often goes away as your body adjusts to treatment. This takes 2-3 months of adaption
  2. Decrease in Pressure Support (PS) or EPR (Expiratory Pressure Relief)/Flex on a CPAP/APAP/BiLevel Device
  3. Decrease in pressure on a CPAP/APAP/BiLevel Device
  4. Anything that decreases the efficiency of your breathing
  5. EERS (Enhanced Expiratory Rebreathing Space) The theory is that the use of positive air pressure, especially with pressure support (PS) or exhale pressure relief (EPR) can result in a drop in carbon dioxide in the blood, which through various respiratory feedback mechanisms can result in the emergence of central apnea (CA). By adding dead-spece or a larger volume EERS does the via a mask modification which slightly increases the amount of CO2 that is rebreathed. This effectively eliminated the central apnea. Note that this is a process that your medical team has not likely heard of and because it requires a mask modification is frowned on by many in the medical profession. I'll add that this process is used extensively by a few doctors in cooperation with a few DMEs and Sleep Centers.


Hypocapnia or hypocapnea (from the Greek words υπό meaning below normal and καπνός kapnós meaning smoke), also known as hypocarbia, sometimes incorrectly called acapnia, is a state of reduced carbon dioxide in the blood. Hypocapnia usually results from deep or rapid breathing, known as hyperventilation.

Physiology of Respiratory Control

Deviations from normal arterial levels of oxygen, carbon dioxide, and pH are sensed by central and peripheral chemoreceptors. The central chemoreceptors are the major sensory organ of arterial carbon dioxide while the peripheral chemoreceptors are most influential in sensing arterial oxygen and pH. These signals are sent to the brainstem respiratory center which in turn signals the muscles of breathing that modify the alveolar ventilation rate. Finally, changes to the alveolar ventilation rate return the arterial oxygen, CO2, and pH levels to their normal values.

Central Apnea is the interruption of this cycle resulting is a pause or temporary stoppage of breathing.

Role of CO2

Changes to the partial pressure of arterial carbon dioxide are sensed by both the central and peripheral chemoreceptors. Increased arterial partial pressures of CO2 strongly stimulates the central chemoreceptors which send level signals to the brainstem respiratory centers that increase respiratory drive. The resultant increase in alveolar ventilation results in pulmonary elimination of carbon dioxide and thus the restoration of lower arterial carbon dioxide levels. Important from a central apnea point of view, a decreased arterial partial pressures of CO2 strongly suppresses the respiratory drive and thus reducing ventilation, allowing for a buildup of arterial carbon dioxide levels.

Role of O2 and pH

Acidosis (decrease in pH) increases respiratory drive, thus increasing ventilation which helps increase the blood pH by breathing off of carbon dioxide. Conversely, alkalosis (increase in pH) decreases respiratory drive, thus decreasing ventilation which helps reduce the blood pH by slowing the elimination of carbon dioxide.

The peripheral chemoreceptors are the only sensory components that directly sense and respond to changes in the oxygen levels. When hypoxemia ensues the peripheral chemoreceptors are strongly activated and increase respiratory drive by activating the respiratory system resulting in increased ventilation thus increasing oxygen levels. It should be noted that this does little to suppress respiration.


Treatment of positive airway pressure treatment-associated respiratory instability with enhanced expiratory rebreathing space (EERS).

Alternative approaches to the treatment of Central Sleep Apnea