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Fully Implantable Miniature Stimulator for Stimulation of Respiration Disclosure Number: IPCOM000021843D
Publication Date: 2004-Feb-11

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Microstimulators are employed which can stimulate both the phrenic nerve and, concurrently, other muscles that are used in respiration. The system and method enable improved simulation of normal respiration, as well as replication of coughing. The microstimulators can coordinate their stimulation of the diaphragm and other respiration muscles through a communication system linking each microstimulator. The use of microstimulators can also reduce surgical trauma associated with implanting large, conventional stimulators.

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Fully Implantable Miniature Stimulator

for Stimulation of Respiration


The present invention relates to artificial ventilation for respiration and more particularly to diaphragmatic pacing through stimulation of the phrenic nerve innervating the diaphragm.

A number of diseases and injuries may rob patients of the ability to breathe on their own. Some of these diseases include muscular dystrophy (MD) with a prevalence of 3-6 per 100,000, amyotrophic lateral sclerosis (ALS) with a prevalence of 11 per 100,000, and multiple sclerosis (MS) with a prevalence of 91.7 per 100,000. These diseases deleteriously affect either the muscles that are used in respiration or the nerves that are connected to these muscles. Injuries that occur can also require artificial ventilation. For instance, stroke patients can have impaired ability to breathe. Moreover, patients with relatively high C4 cervical spinal cord injuries (SCI) cannot breathe on their own.

A respiratory cycle has both an inspiratory and an expiratory phase. At a rest state, the inspiratory phase lasts about one second, while the expiratory phase lasts about three seconds. During inspiration there is an increase in the thoracic capacity reducing the intra-pleural pressure, expanding the lungs and decreasing intrapulmonary pressure, thereby drawing air into the respiratory passages. The expiratory phase is largely passive, wherein the recoil of the thoracic wall and lungs raises the intra-thoracic pressure and expels the air from the lungs.

The contraction of muscles that effect respiration are generally controlled by the phrenic and intercostal nerves. The ipsilateral phrenic nerve passes the cervical plexus, enters the thorax and passes to the diaphragm. The phrenic nerve therefore controls the diaphragm.

During quiet breathing, e.g., at rest, the diaphragm is the predominant active muscle which produces respiration. As the diaphragm contracts, the pleural pressure drops, which lowers the alveolar pressure and draws air in from the mouth to the alveoli. Expiration during quiet breathing is essentially a passive phenomenon. As the respiratory muscles relax, the elastic lung and chest wall return passively to their resting volume (the functional residual capacity).

However, during exercise, many other muscles, in addition to the diaphragm also become active. During inspiration, the external intercostals raise the lower ribs up and out, which increases the lateral and antero-posterior dimensions of the thorax. The scalene muscles and sternocleidomastoids are also active, raising and pushing out the upper ribs and the sternum.

During active expiration, the most important muscles are those of the abdominal wall, including the rectus abdominis, internal and external obliques, and transversus abdominis, which through their contraction, drive the intra-abdominal pressure up. At the same time, the diaphragm pushes up, raising the pleural pressure, in turn, raising alveolar pressure, causing t...