Why correct nocturnal dyspnea in heart failure?

The coexistence of respiratory disease with cardiovascular and cerebrovascular disease used to be explained on the basis of shared risk factors, such as age, gender, and obesity. However, recent large-scale systematic epidemiological studies have shown that sleep-related breathing disorders are independent risk factors for hypertension, probably due to a combination of intermittent hypoxia and hyper-capnia, arousal, increased sympathetic tone, and altered baroreflex control during sleep. Occurring in 40% to 60% of heart failure patients, they comprise central sleep apnea, also known as Cheyne-Stokes respiration (CSR), in 36% of cases, obstructive sleep apnea in 12%, and a combination of central and obstructive dyspnea in the remainder.

When Cheyne (1818) and later Stokes (1854) described abnormal breathing in heart failure, the pattern that they observed in patients who were awake was agonal, or ante-mortem, breathing. CSR is now considered as a consequence of heart failure, more common in men than in women. It causes sleep fragmentation and a decrease in rapid-eye movement sleep, hence tiredness. The pathophysiology is incompletely understood. Proposed mechanisms include increased ventilatory response to minor changes in blood gases, underdamping of the ventilatory response, and a circulatory time delay between the lungs and central and peripheral chemoreceptors. Respiratory muscle weakness is a contributory mechanical factor in heart failure patients. The natural arterial oxyhemoglobin desaturation caused by sleep-disordered breathing also accelerates heart failure progression, particularly as it has been associated with excess mortality in patients with chronic obstructive pulmonary disease.

Central sleep apnea is considered an independent marker for increased mortality in congestive heart failure. Because such breathing disorders make intense mechanical and adrenergic demands on the failing myocardium that cannot be reversed by conventional pharmacological therapy, their diagnosis and correction is integral to the optimal management of heart failure. Thus, the abolition of obstructive sleep apnea by mechanical positive airway pressure significantly improved heart failure symptoms and left ventricular ejection fraction after 1 month.

Central sleep apnea in congestive heart failure arises from hypocapnia during sleep. Since PaC02 approximates to the apneic threshold, only a slight increase in ventilation is sufficient to drive PaCO, below the apneic threshold and trigger central apnea, as in the response to arousal. This, in turn, precipitates hypoxic dips. Unless these dips are quite pronounced, it is unlikely that the relief of hypoxia would depress C02 drive sufficiendy to allow PaC02 to rise above the apneic threshold.

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