Surgery – Respiratory method or device – Means for supplying respiratory gas under positive pressure
Reexamination Certificate
2000-02-03
2004-06-22
Lo, Weilun (Department: 3761)
Surgery
Respiratory method or device
Means for supplying respiratory gas under positive pressure
C128S204210
Reexamination Certificate
active
06752150
ABSTRACT:
BACKGROUND OF THE INVENTION
Central sleep apnea is a type of sleep-disordered breathing that is characterized by a failure of the sleeping brain to generate regular, rhythmic bursts of neural activity. The resulting cessation of rhythmic breathing, referred to as apnea, represents a disorder of the respiratory control system responsible for regulating the rate and depth of breathing, i.e. overall pulmonary ventilation. Central sleep apnea should be contrasted with obstructive sleep apnea, where the proximate cause of apnea is obstruction of the pharyngeal airway despite ongoing rhythmic neural outflow to the respiratory muscles. The difference between central sleep apnea and obstructive sleep apnea is clearly established, and the two can co-exist. While central sleep apnea can occur in a number of clinical settings, it is most commonly observed in association with heart failure or cerebral vascular insufficiency. An example of central sleep apnea is Cheyne-Stokes respiration.
The respiratory control system comprises a negative feedback system wherein a central pattern generator creates rhythmic bursts of activity when respiratory chemoreceptors sensing carbon dioxide, oxygen and pH are adequately stimulated (FIG.
1
). While this neural output of the brainstem central pattern generator to the respiratory muscles derives from a neural rhythm generated intrinsically by the central pattern generator, the generator becomes silent if the feedback signals, related to arterial P
CO2
and P
O2
, are not sufficiently intense. In other words, the respiratory rhythm is generated by a conditional central pattern generator which requires an adequate input stimulus derived from peripheral chemoreceptors sensing arterial P
CO2
and P
O2
from central chemoreceptors sensing brain P
CO2
/pH. Furthermore, the intensity of neural activity generated by the respiratory central pattern generator depends directly upon the arterial P
CO2
inversely on the arterial P
O2
. Thus, the central and peripheral chemoreflex loops constitute a negative feedback system regulating the arterial P
O2
and P
CO2
, holding them constant within narrow limits (FIG.
1
).
This normal regulation of arterial blood gases is accomplished by a stable ventilatory output of the respiratory central pattern generator. By contrast, central sleep apnea represents an instability of the respiratory control system. The instability can arise from one of two mechanisms, namely: (1) intrinsic failure of the respiratory central pattern generator in the face of adequate stimulation by respiratory chemoreceptors; or (2) lack of adequate stimulation of the central pattern generator by respiratory chemoreceptors. The former is referred to as the “intrinsic instability” and the latter is referred to as the “chemoreflex instability.” Theoretically, both mechanisms can co-exist. The common form of central sleep apnea is thought to be caused by the chemoreflex instability mechanism.
The chemoreflex control of breathing might exhibit instability either because the delay of the negative feedback signal is excessively long or because the gain of the system is excessively high. Current evidence indicates that the latter constitutes the principal derangement in central sleep apnea caused by heart failure. Specifically, the overall response of the control system to a change in arterial P
CO2
is three-fold higher in heart-failure patients with central sleep apnea than in those having no sleep-disordered breathing. This increased gain probably resides within the central chemoreflex loop; however, high gain of the peripheral chemoreflex loop cannot be excluded. Accordingly, the fundamental mechanism of central sleep apnea is taken to be high loop gain of the control system, which results in feedback instability during sleep.
Central sleep apnea causes repeated arousals and oxyhemoglobin desaturations. Although firm evidence linking central sleep apnea to morbidity and mortality is lacking, a variety of evidence leads to the inference that central sleep apnea may promote cardiac arhythmias, strokes, or myocardial infarctions. The repeated nocturnal arousals are likely to impair daytime cognitive function and quality of life. No treatment has become established as being effective for central sleep apnea. Stimulating drugs such as theophyline may be helpful, and carbonic anhydrase inhibitors may relieve central sleep apnea in normals sleeping at high altitude. Nasal continuous positive airway pressure may directly or indirectly improve ventilatory stability. Increasing inspired fractional concentration (F) of oxygen in the inspired gas generally does not eliminate central sleep apnea, whereas increasing inspired F
CO2
(F
ICO2
=0.01-0.03) promptly eliminates central sleep apnea. However, long-term exposure to high F
ICO2
would appear to be an undesirable long-term therapy.
SUMMARY OF THE PRESENT INVENTION
The present invention is a method for varying the efficiency of pulmonary gas exchange by using a controlled amount of rebreathing during certain periods of the central sleep apnea respiration cycle so as to counteract the effects of the transient excessive ventilation on the level of carbon dioxide and oxygen in the lungs and in the arterial blood. In effect, this strategy is an attempt to stabilize breathing by minimizing oscillations in the feedback variables.
The invention counteracts periodic breathing due to central sleep apnea by decreasing loop gain of the respiratory control system. In one embodiment, the invention dynamically modulates efficiency of pulmonary gas exchange in relation to pulmonary ventilation. When pulmonary ventilation is stable at resting values, the performance of the system is unchanged. However, during a period of hyperpnea, i.e. when ventilation increases transiently to supra-normal levels, the system is made more inefficient, thus decreasing loop gain and stabilizing the system.
Rebreathing can be used to increase the inspired percentage carbon dioxide and reduce the inspired percentage oxygen just before or during the period of overbreathing. In one embodiment, the patient's ventilation is continuously monitored and analyzed in real time so that the ventilation periodicities of the central sleep apnea breathing can be detected and the inspired carbon dioxide and oxygen concentrations adjusted appropriately by varying the amount of exhaled gas that is reinspired.
In another embodiment of the present invention, a rebreathing apparatus is a part of a nasal continuous positive airway pressure (CPAP) system. The use of continuous positive airway pressure may have a beneficial effect on cardiac function in patients with congestive heart failure. In the future it is likely that patients with congestive heart failure will receive nasal CPAP for treatment of the heart failure. Central sleep apnea may not immediately disappear upon administration of conventional nasal CPAP therapy as central sleep apnea respiration is basically of a non-obstructive origin. However, over a period of about four weeks the degree of heart failure improves; thus, the resulting central sleep apnea respiration may be relieved by the continuous positive airway pressure. This is described in the papers, Naughton, et al., “Effective Continuous Positive Airway Pressure on Central Sleep Apnea and Nocturnal Percentage Carbon Dioxide in Heart Failure,” American Journal Respiratory Critical Care Medicine, Vol. 1509, pp 1598-1604, 1994; Naughton, et al., “Treatment of Congestive Heart Failure and Central Sleep Apnea Respiration during Sleep by Continuous Positive Airway Pressure,” American Journal of Critical Care Medicine, Vol. 151, pp 92-97, 1995; and, Naughton, et al., “The Role of Hyperventilation in the Pathogenesis of Central Sleep Apneas in Patients with Congestive Heart Failure,” American Review of Respiratory Diseases, Vol. 148, pp 330-338, 1993.
It is desirable to have a prompt elimination of the central sleep apnea respiration because the resulting daytime sleepiness and impaired cognition resulting from repeated arousals impair the pati
Hajduk Eric A.
Platt Ronald S.
Remmers John E.
Lo Weilun
Mitchell Teena
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