Tetraplegia is a risk factor for central sleep apnea

Abstract

Sleep-disordered breathing (SDB) is highly prevalent in patients with spinal cord injury (SCI); the exact mechanism(s) or the predictors of disease are unknown. We hypothesized that patients with cervical SCI (C-SCI) are more susceptible to central apnea than patients with thoracic SCI (T-SCI) or able-bodied controls. Sixteen patients with chronic SCI, level T6 or above (8 C-SCI, 8 T-SCI; age 42.5 ± 15.5 years; body mass index 25.9 ± 4.9 kg/m(2)) and 16 matched controls were studied. The hypocapnic apneic threshold and CO2 reserve were determined using noninvasive ventilation. For participants with spontaneous central apnea, CO2 was administered until central apnea was abolished, and CO2 reserve was measured as the difference in end-tidal CO2 (PetCO2) before and after. Steady-state plant gain (PG) was calculated from PetCO2 and VE ratio during stable sleep. Controller gain (CG) was defined as the ratio of change in VE between control and hypopnea or apnea to the ΔPetCO2. Central SDB was more common in C-SCI than T-SCI (63% vs. 13%, respectively; P < 0.05). Mean CO2 reserve for all participants was narrower in C-SCI than in T-SCI or control group (-0.4 ± 2.9 vs.-2.9 ± 3.3 vs. -3.0 ± 1.2 l·min(-1)·mmHg(-1), respectively; P < 0.05). PG was higher in C-SCI than in T-SCI or control groups (10.5 ± 2.4 vs. 5.9 ± 2.4 vs. 6.3 ± 1.6 mmHg·l(-1)·min(-1), respectively; P < 0.05) and CG was not significantly different. The CO2 reserve was an independent predictor of apnea-hypopnea index. In conclusion, C-SCI had higher rates of central SDB, indicating that tetraplegia is a risk factor for central sleep apnea. Sleep-related hypoventilation may play a significant role in the mechanism of SDB in higher SCI levels.

Diagnostic accuracy of a two-stage model for detecting obstructive sleep apnoea in chronic tetraplegia

“…While central sleep apnoea has previously been identified in tetraplegia,38 our data suggest that it is not the predominant characteristic of sleep disordered breathing, accounting for just 4% of the classified events on average. Only 2% of our combined sample (3/178) had predominant central sleep apnoea.…”

Neuropsychological Function in Patients With Acute Tetraplegia and Sleep Disordered Breathing

“…4 Up to 91% of patients with complete tetraplegia have SDB, despite few being clinically suspected of the disease. 5,6 Several mechanisms for SDB following tetraplegia have been proposed, such as increased upper airway resistance, 4 impaired respiratory feedback from the rib cage, 4 alterations in ventilatory control and plant gain, 7 and diminished activation of intercostal, abdominal, and diaphragm muscles. 4,8 In chronic tetraplegia, sleep onset hypoventilation, 9 obstructive, 7 and central apneas 7 have all been reported, 10 while in acute tetraplegia, obstructive and mixed events appear to predominate.…”

“…5,6 Several mechanisms for SDB following tetraplegia have been proposed, such as increased upper airway resistance, 4 impaired respiratory feedback from the rib cage, 4 alterations in ventilatory control and plant gain, 7 and diminished activation of intercostal, abdominal, and diaphragm muscles. 4,8 In chronic tetraplegia, sleep onset hypoventilation, 9 obstructive, 7 and central apneas 7 have all been reported, 10 while in acute tetraplegia, obstructive and mixed events appear to predominate. 3,11,12 Reports, however, in both the acute and chronic, vary in methodology, scoring criteria, and participant characteristics, such that a clear pattern of the nature of SDB remains controversial.…”

Sleep‐disordered breathing in heart failure: facts and numbers

“…The patency of the respiratory tract is functional, but the ventilatory effort, the essential central trigger for breathing, is intermittently disrupted. This malfunction can originate from a variety of neurological diseases11, 12, 13, 14 or HF 1, 3, 5, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24. In HF, the accepted hypothesis is that pulmonary congestion, (which is further aggravated in a horizontal sleeping position) due to a higher left ventricular filling pressure, activates lung vagal irritant receptors causing hyperventilation and hypocapnia 3, 5, 19.…”