Posted by Greg Harper on April 14, 1998 at 20:02:09:

In Reply to: Central Sleep Apnea posted by Edie Country on April 10, 1998 at 23:45:56:

Dear Edie:

Laryngospasm occurs when the nerve that controls the vocal cords (laryngeal nerve)is over-stimulated by a number of different physical factors. 99.99% of the time the spasm
is relatively short in duration (less than one minute) but the after effects of the airway
blockage, shortness of breath and respiratory distress, can last for several minutes until
the body can compensate for the physiologic stress that is caused by the event.

The fact that the spasm is of short duration is of little matter to the person who is having
the attack. They can be truly frightening events because you can’t get air in or out of the
airway and the person who is experiencing the spasm has no idea how long it will last.

The larynx is the gateway to the trachea (windpipe) and the lungs. One of the functions
of the vocal cords, besides speech, is to protect the lower airway from aspirating
(inhaling) foreign objects that could get down into the bronchus and bronchioles to cause
blockage and/or infection. These muscles are very quick to react and close off the airway
but they do not have a great deal of endurance so they can’t stay contracted for very long.

Now...how does sleep apnea set off a laryngospasm.

During an apneic event, whether it is central of obstructive, the body continues to produce carbon dioxide (CO2) and use up oxygen (O2). Both of these gases are powerful stimulants for breathing. In adults, elevated CO2 levels are the first to create a stimulus to breathe. The body continuously produces CO2 and uses up O2 during metabolism so that while the apnea event is taking place the stimulus to breathe gets greater and greater. The apnea event can last for a few seconds up to minutes in some individuals. The longer the apnea event, the greater the drive to breathe. Finally, the individual arouses from
sleep, there is a tremendous drive to breathe built-up and the person will gasp to exchange air, then awakening occurs.

The peak inspiratory airflow’s can get very high, somewhere in the range of 200 - 300 liters per minute (possibly higher). This high inspiratory airflow can not only stimulate laryngospasm by it’s sheer velocity, but it can also physically move sputum from the pharynx down into the larynx to stimulate spasm.

During the apnea event there can also be very large changes in intrathoracic (inside the
chest) pressure. I suspect that these large pressure changes can be enough to stimulate the
glossopharyngeal and vagus nerves which would then stimulate the laryngeal nerve in some individuals. Laryngospasm would then result.

I would suspect that once the apnea is treated the episodes of laryngospasm would immediately abate unless the is some other undiagnosed and co-existing condition that is causing them.

Pure central sleep apnea (CSA) is less frequently seen than obstructive sleep apnea (OSA). Most people, your husband included, have a combination of central and obstructive sleep apnea.

CSA occurs when the area of the brain that controls breathing, for some reason, does not
tell the muscles of respiration to work. Or, it can be that the brain sends the signal and
the respiratory muscles just don’t receive the message.

CSA will sometimes be greatly reduced when OSA is treated or it may require a different type of machine (BiLevel as opposed to CPAP) to treat the CSA. Either way both conditions are completely treatable and one is no more dangerous than the other.

When your husband has his second sleep study done, the sleep lab staff will determine which therapy to use.

I hope that this has answered some of your questions.

Sincerely,

Gregory Harper, RRT, RCP
Respiratory Care Practitioner

Follow Ups:

• Re: Central Sleep Apnea Ranald Bruce 4/20/98 (1)
  • Re: Central Sleep Apnea Greg Harper 4/20/98 (0)

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