Cheyne-Stokes respiration (CSR) is a form of periodic breathing that offers during sleep in some patients with congestive heart failure (CHF)[1] It was originally described throughout 170 years ago[2.

Cheyne-Stokes respiration (CSR) is a form of periodic breathing that offers during sleep in some patients with congestive heart failure (CHF)[1] It was originally described throughout 170 years ago[2,3] and has been recognized as a cause of repose disruption[4,5] and possibly an indicator of poor prognosis in patients with left ventricular dysfunction.[6] The pathogenesis of periodic breathing has been investigated extensively[7-11] and is related to the following: (1) los of behavioral stimulation of respiration at be still onset; (2) alteration of the apnea door which is the arterial [Pcosub2] ([PaCO.sub.2]) below which apnea be founds on transition from wakefulness to sleep; (3) the evolution of hypoxema that increases gain and decreases dampening of metabolic control of respiration; and (4) circulatory delay between the lung and carotid dead body that delays the ventilatory replication to changes in arterial [Posub2] and [Pcosub2]

Although CSR is associated with left ventricular dysfunction, it does not meet the eye in all patients with CHF Cheyne-Stokes respiration fall outs predominantly during nonrapid eye move (NREM) sleep, particularly stage 1 and 2[4] during which breathing is normally regulated by means of changes in [PaCO.sub.2].[12,13] If [PaCO.sub.2] falls below the critical even required for the generation of respiratory periodical emphasis (apnea threshold) during NREM repose apnea ensues. Sleep attack is associated not only with los of waking neural respiratory drive moreover also with elevation of the apnea threshold[9] Consequently be dead onset in a hypocapneic individual may terminate in apnea, and persistent oscillation of [PaCO.sub.2] above and below the apnea opening may lead to periodic breathing. Awake hypocapnia has frequently been reported in patients with CSR[41415] possibly suitable to stimulation of pulmonary mechanoreceptors according to interstitial edema. Consequently, we hypothesized that CHF patients with awake hypocapnia are more likely to expand CSR during sleep. We addressed this hypothesis at comparing the cardiorespiratory profiles, particularly transcutaneous [Pcosub2] (tc [Pcosub2]) during nap and wakefulness, of CHF patients with and without CSR

METHODS

Patient Population

We studied 16 consecutive patients with strait-laced stable CHF (New York Heart Association [NYHA] class 3 to 4) whose resting left ventricular ejection fraction (LVEF) was [les than] 35 percent A history of abnormal breathing during be still was not required for hall into the study. Patients were exclud if they had the following: (1) significant pulmonary, renal, or neurologic disease; (2) medication prescribed that alters respiratory drive; and (3) carbon dioxide retention, defined as awake [PaCO.sub.2] [greater than] 45 mm Hg Each patient had an overnight nap study. The following day, pulmonary function ordeals chest radiograph, radionuclide angiography, and echocardiography were performed. The protocol was approved from the ethics committee of our institution and informed assent was obtained from each patient.

be still Study

The following variables were monitored during overnight polysomnography. We recorded two-channel electroencephalogram (EEG) ([Csub3] - [A.sub.2], [Csub4] - [A.sub.1]), electro-oculogram (EOG) and submental electromyogram (EMG) using surface electrode Airflow was descryed by monitoring expired [CO.sub.2] at the nose and inlet through nasal cannulas adapted for this end and attached to a [COsub2] analyzer (PB 223 Puritan-Bennett Corporation). Respiratory effort was monitored according to respiratory plethysmography with transducers placed around the chest and abdomen (Respitrace, Ambulatory Monitoring, Ardsley, NY) Arterial oxygen saturation ([SaO.sub.2]) was recorded with a oscillation oximeter (Biox 3740, Ohmeda, Boulder Colo) appoint at its fastest response. Transcutaneous [Pcosub2] (tc [Pcosub2]) was recorded from a [Pco.sub.2] sensor placed onward the anterior chest wall and attached to a [COsub2] monitor (Kontron 7640 Medilog Ltd) The ECG and heart rate were recorded from standard limb leads. All variables were continuously recorded upon a polygraph (model 78E, Grass Instruments, Quincy, Mass) at a paper spe of 10 mm/ Transcutaneous [Pcosub2] was displayed upon a slow recorder (paper spe 20 cm/h) that was synchronized to the polygraph (Grass).

All polysomnograms were scored manually and nap stage and arousals were determined by the agency of established criteria using the EEG EOG and EMG[16] An arousal was defined as an awakening from slumber for more than 5 s as evidenced by simultaneous [alpha] activity upon the EEG, EMG activation, and vigilance movements. Central apnea was defined as absence of airflow for more than 10 s due to loss of respiratory effort. Hypopnea was defined as a reduction in the amplitude of respiratory effort of at least 50 percent from the sleeping baseline of the same height for more than 10 s The apnea-hypopnea index (AHI) was defined as the number of apneas and hypopneas by hour of sleep. Cheyne-Stokes respiration was defined as periodic breathing with alternating central apnea or hypopnea and hypernea in a crescendo/descrescendo pattern and the duration of CSR was signifyed as a percentage of total be still time (percent TST). Oxygen saturation during rest was expressed in three ways: (1) duration of oxygen saturation [les than] 90 percent uttered as a percent TST; (2) mean oxygen saturation (mean [SaO.sub.2]), calculated by means of averaging the high and grave [SaO.sub.2] for each 30-s epoch; and (3) mean minimum (min [SaO.sub.2]) that was determined from the lowest [SaO.sub.2] for each point [i]or[/i] period of time In addition, mean oxygen saturation during all periods of wakefulness ([SaO.sub.2] [W]) was calculated on averaging high and low [SaO.sub.2] for each 30- period of wakefulness. Transcutaneous [Pcosub2] was measured during three different conditions: (1) mean tc [Pcosub2] during 5 to 15 min of wakefulness at the beginning of the studious mood (tc [Pco.sub.2] [[W.sub.1]]); (2) mean tc [Pcosub2] during all periods of wakefulness (tc [Pcosub2] [W]); and (3) mean tc [Pcosub2] during doze (tc [Pco.sub.2] [TST]). All mean values of tc [Pcosub2] were calculated from the average tc [Pcosub2] across 36-s intervals.

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