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Central Sleep Apnea in Heart Failure
Figure 1: Fragment from a Polysomnographic Recording of a Patient with Heart Failure and Central Sleep Apnea
LOC
ROC
Chin EMG
C3-A2
O2-A1
ECG
Nasal flow
Thoracic effort
Abdominal effort
Oximetry
989898 97 9797 97
9696 9595 9594
9494 94 9393 93 92
95 92 92 90 9090
89 89 87
87
LOC = left eye occulogram; ROC = right eye occulogram; EMG = electromyography; C3–A2 and O2–A1 = elecetroencphalogram channels; ECG = electrocardiogram; nasal flow is derived from nasal
pressure; abdominal and chest effort are measured by standard plesthysmography. The recording is a compressed 120-second epoch. Note that the breathing pattern demonstrates a
crescendo–decrescendo ventilation followed by central apneas (no abdominal or thoracic effort). The morphology of the breathing pattern is consistent with Cheyne-Stokes respiration. This
disorder is classified as central sleep apnea based on this sleep study. Intermittent hypoxia is also noted in the oximetry signal with the central events.
It is imperative at this point to note that at the end of a central apnea, a hyperventilation characterized by close proximity between their baseline
decrease in upper airway tone occurs.
15
Thus, obstruction of the upper sleep (eupneic) level of PaCO
2
(steady-state level of ventilation) and their
airway is part of the mechanism of central apnea. One patient can apnea threshold.
18
The mechanism of this chronic hyperventilation in
manifest mixed, central, and obstructive events during a single night. It patients with heart failure is thought to be related to pulmonary interstitial
is therefore sometimes overly and inappropriately simplistic to consider congestion.
19,20
In animal models, respiratory control instability and central
a particular patient’s respiratory sleep disorder as one or the other and apnea were induced in response to increased left atrial pressure.
21
This is
not a combined central and OSA disorder. a typical condition in patients with systolic dysfunction, and is more likely
when they assume the supine position during sleep.
22
Mechanism of Central Sleep Apnea
As cardiac systolic function deteriorates, several pathophysiological Any slight increase in ventilation during sleep, as occurs with arousal or
conditions develop and contribute to both respiratory control instability changes in sleep stage, will result in a drop in PaCO
2
below the apnea
and reduced upper airway patency, subsequently promoting both threshold, precipitating apneic events.
23
Given the inertia in the
obstructive and central respiratory events during sleep. The following respiratory control system,
24
breathing does not resume until an
discussion of the mechanism of CSA is brief and will focus on recent excessive chemical stimulus (hypercapnea) has accumulated, producing
developments. The topic has been fully reviewed recently.
16,17
an ‘overshoot’ of ventilation that is likely to drop PaCO
2
below the apnea
threshold again and propagate periodic breathing and CSR. The
Respiratory Control Instability in Heart Failure chemoreceptor’s response to hypercapnea is increased in patients with
During sleep, the organism’s metabolic rate is slow and stable, and CO
2
heart failure and CSA
25
and their eupeic PaCO
2
is close to their apnea
production is subsequently at a steady sate. Behavioral control of threshold, making this mechanism likely.
18,26
breathing is abolished by the sleep state, and the arterial carbon dioxide
level (PaCO
2
) becomes the main stimulus for ventilation. As such, Changes in cerebral perfusion (cerebrovascular reactivity) in response
respiration ceases if PaCO
2
falls below a tightly regulated level called the to changes in PaCO
2
play an important role in the ventilatory response of
apnea threshold. Patients with heart failure have a pattern of chronic the central chemoreceptors. Normally, an increase in PaCO
2
(i.e. during
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