Central Sleep Apnea

Abstract

Neurophysiologically, central apnea is due to a temporary failure in the pontomedullary pacemaker generating breathing rhythm. As a polysomnographic finding, central apneas occur in many pathophysiological conditions. Depending on the cause or mechanism, central apneas may not be clinically significant, for example, those that occur normally at sleep onset. In contrast, central apneas occur in a number of disorders and result in pathophysiological consequences. Central apneas occur commonly in high-altitude sojourn, disrupt sleep, and cause desaturation. Central sleep apnea also occurs in number of disorders across all age groups and both genders. Common causes of central sleep apnea in adults are congestive heart failure and chronic use of opioids to treat pain. Under such circumstances, diagnosis and treatment of central sleep apnea may improve quality of life, morbidity, and perhaps mortality. The mechanisms of central sleep apnea have been best studied in congestive heart failure and hypoxic conditions when there is increased CO2 sensitivity below eupnea resulting in lowering eupneic PCO2 below apneic threshold causing cessation of breathing until the PCO2 rises above the apneic threshold when breathing resumes. In many other disorders, the mechanism of central sleep apnea (CSA) remains to be investigated.

The Management of Co-Morbidities in Patients with Heart Failure – Central Sleep Apnoea

“…Repeated cycles of apnoea, hypoxia, and arousal during sleep impart significant cardiovascular insults such as additional sympathetic nervous system activation, acute pulmonary and systemic hypertension, plaque rupture and arrhythmias. [1,[29][30][31] As the cycles continue, these insults continue to adversely affect the heart and contribute to the downward cycle of HF including an increased risk for recurrent HF hospitalizations, ventricular arrhythmias and mortality ( Figure 1). [3,6] Identifying heart failure patients with CSA…”

Sleep disordered breathing in patients with heart failure

“…HCSB occurs in patients with HF both during the day and at night, but CSA occurs only during sleep or when the patient is dozing. Pathological mechanisms underlying CSA have been widely investigated within last decade and explained in detail in a recent monograph [24]. The important factors involved in pathophysiology of CSA are: diminished PCO 2 reserve (difference between eupneic PCO 2 and apnea threshold) [24, 25], and augmented central and peripheral hypoxic and hypercapnic chemosensitivity [26,27].…”

“…In response to pulmonary congestion vagus nerve becomes activated (by non-myelinated type C nerve fi bers in parenchyma of the lungs, in alveolar bronchioles, alveolar capillaries and distention-sensitive receptors), that leads to central activation of breathing. Meanwhile, pulmonary congestion also decreases the PCO 2 reserve and predisposes to central apnea [24], this by mechanisms not fully explained. Therefore, during sleep, even a slight increase in ventilation caused by arousal or changes in position may lead to a drop in PCO 2 below the apnea threshold and results in occurrence of apnea episode.…”

“…Cessation of breathing leads to accumulation of CO 2 which is the chemical stimulus for resumption of ventilation. Enhanced chemoreceptor sensitivity propagates excessive ventilation and subsequent drop in PCO 2 below apnea threshold and the next apnea [1,2,24,26]. The duration of the cycle of periodic breathing is proportional to circulation time from lung to chemoreceptors.…”

“…It has been suggested [2,24] that lack of increase in PCO 2 results from inability to decrease ventilation that normally occurs at sleep onset. Patients with HF, particularly those with severely impaired diastolic function, may develop an increase in pulmonary capillary pressure due to increased venous return, which in turn refl exively increases respiratory rate and ventilation at sleep onset.…”