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Figure 2: Conceptualization of the Cardiovascular Consequences of Central Sleep Apnea in Patients with Heart Failure
Increased dystolic Increased venous return Pulmonary
transmural pressure right ventricular overload
Increased cardiac work index Impaired left ventricular filling
to endothelial cells
Endothelial Impaired diastolic
Reduced stroke volume Increased right
and cardiac output ventricular afterload coronary perfusion
• Pulmonary edema
• Increased circulatory delay
• Increased ventilatory drive
• Decreased cerebral blood flow
RV = right ventricle; LV = left ventricle; OSA = obstructive sleep apnea; CSA = central sleep apnea.
apnea) produces cerebrovascular dilation, while a decrease in PaCO
(i.e. Increased pulmonary vascular congestion is thought to contribute to
post-apnea hyperventilation) produces cerebrovascular constriction. The hyperventilation and increased respiratory control instability, leading
normal decrease in cerebral perfusion with hypocapnea (which occurs to CSA.
Studies also suggest that cervical venous congestion may
during the hyperventilation phase of CSR) allows for greater equally destabilize the upper airway and potentially produce obstructive
accumulation of CO
at the level of central chemoreceptors. events as well.
It is known that CSA may result from upper airway
This subsequently allows for continued stimulus to breathe and possibly instability
and that upper airway obstruction may follow central
decreases the potential for or duration of apnea. apnea.
Worsening of heart failure may therefore lead to both increased
central and obstructive apneas.
Similarly, the cerebrovascular dilation that occurs with hypercapnea
can produce a ‘wash-out’ effect at the level of the central Consequences of Central Sleep Apnea
chemoreceptors. This decreases the accumulation of CO
following an in Heart Failure
apnea and prevents the expected ventilatory overshoot, therefore CSA is a manifestation of respiratory control instability in patients with
decreasing the likelihood that an apnea will ensue.
Patients with heart severe systolic dysfunction. Once present, however, CSA is associated
failure have a reduced cerebrovascular response to changes in PaCO
. with a set of neurocirculatory responses that are detrimental for the
This reduces the ability of the respiratory control center to dampen the failing heart. The recurrence of central respiratory events followed by
overshoot and undershoot in the ventilatory response to CO
a recovery phase induces a cyclical pattern of intermittent
hypoxia–reoxygenation. Evidence from experimental human and
Central Sleep Apnea, Mixed Sleep-disordered animal studies has demonstrated that intermittent hypoxia is the
Breathing, and Systolic Heart Failure critical lesion accounting for this cascade of the neurocirculatory
The role of increased filling pressure in the pathogenesis of SDB in response to SDB. Figure 2 summarizes the mechanisms discussed
patients with heart failure is intriguing and only minimally understood. in this section.
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