Herzinsuffizienz und zentrale Atemregulationsstörungen

Zusammenfassung:

Etwa die Hälfte aller Patienten mit fortgeschrittener Linksherzinsuffizienz weisen zentrale Atemregulationsstörungen im Schlaf, meist in Form des Cheyne-Stokes Atemmusters, auf.

Dabei handelt es sich um wiederholte Zyklen mit Apnoe, kontinuierlich ansteigendem Atemzugvolumen bis zur Hyperventilation, dann decrescendoartige Abnahme der Atemtiefe bis zum Atemstillstand. Zentrale Atemregulationsstörungen gelten als unabhängiger, negativer Prognosefaktor für Patienten mit Linksherzinsuffizienz. Während der Apnoen kann es zu kritischen Abfällen der Sauerstoffsättigung im Blut und im Gewebe kommen. Das Wiedereinsetzen der Ventilation ist meist mit Arousals assoziiert, die zur langanhaltenden Aktivierung des Sympathikus führen können. Erhöhte Katecholaminkonzentrationen und die damit verbundene, dauerhaft erhöhte Herzarbeit sind mit einer progredienten Verschlechterung der Herzleistung assoziiert. Möglicherweise verursachen Katecholamine eine Steigerung der Kohlendioxid-Wahrnehmung im rückgekoppelten System der Atmungsregulation. Die gesteigerte CO₂ Wahrnehmung führt zur latenten Hyperventilation und zum schnellen Erreichen der Apnoeschwelle. Als weitere Faktoren für die Entstehung der Cheyne-Stokes Atmung werden eine verlängerte Kreislaufzeit und verminderte Bestände an Kohlendioxid im Körper diskutiert. Die bestevaluierte Therapie ist nCPAP Beatmung, die jedoch von vielen Patienten mit zentralem Schlaf-Apnoe-Syndrom schlecht toleriert wird. Zukünftige Behandlungsstrategien könnten die nichtinvasive Beatmung mit alternativen Beatmungsmustern und die pharmakologische Beeinflussung der Kohlendioxidrezeption umfassen.

Cardiac Insufficiency and Disturbed Central Respiratory Regulation: Cheyne-Stokes Respiration During Sleep in Advanced Left Heart Insufficiency:

Central sleep apnoea, especially Cheyne-Stokes respiration, is found in 45 to 66 % of patients with congestive heart failure (CHF) in functional classes NYHA II to IV. Cheyne-Stokes breathing cycles are characterised by central apnoeas, followed by a crescendo - like increase of tidal volume into hyperventilation and a subsequent decline of tidal volume, ending in another central apnoea. Cheyne-Stokes respiration has been shown to be a poor prognostic factor for patients with CHF.

Apnoeas and hypopnoeas cause marked oxygen desaturation and rises of carbon dioxide concentrations in the blood. The resumption of breathing is frequently associated with arousals, which might cause daytime symptoms like fatigue and sleepiness as well as persistent activation of the sympathetic nervous system. Elevated concentrations of catecholamines increase cardiac work, adversely affecting cardiac function. Serum catecholamines are known to augment the chemoreceptor susceptibility for carbon dioxide. This might be one reason for the permanent mild hyperventilation found in these patients during wakefulness. Increased chemoreceptor responsiveness destabilises the feedback control of breathing, and hyperventilation below the apnoeic threshold grows more likely. Other contributing factors for the development of Cheyne-Stokes respiration include alterations in the control of breathing during sleep and the increased circulation time between the lung and chemoreceptors in CHF patients. The feedback regulation of breathing might be less dampened since carbon dioxide levels are reduced in these patients.

Treatment includes nCPAP, but in many cases this is poorly tolerated in patients with central sleep apnoea. Future approaches to Cheyne-Stokes respiration might focus on improving ventilatory pattern and pharmacological manipulation of carbon dioxide receptor susceptibility.

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