Zusammenfassung
Alleine in Deutschland leiden mindestens 500.000 Menschen an dem durch die Leitsymptome Tagesmüdigkeit, morgendliche Kopfschmerzen und nächtliches Schnarchen charakterisierten obstruktiven Schlafapnoesyndrom (OSAS). Dabei ist die Prognose mutmaßlich durch kardiovaskuläre Komplikationen bestimmt. Während es bei diesen Patienten regelhaft während der Nacht zu pulmonalarteriellen Druckerhöhungen kommt, besteht bei etwa jedem 5. Patienten eine am Tage persistierende pulmonalarterielle Hypertonie, bei jedem 4.—am ehesten als Folge der nächtlichen Druckerhöhung—eine eingeschränkte rechtsventrikuläre Funktion. Tierexperimentelle und klinische Studien konnten darüber hinaus zeigen, dass die intermittierende Hypoxie mit der Entwicklung einer Rechtsherzhypertrophie assoziiert ist. Die funktionelle Ventrikeldynamik unterscheidet sich grundlegend zwischen linkem und rechtem Herzen. Die rechtsventrikuläre Funktion ist wesentlich durch Druckänderungen und nur in geringem Ausmaß durch Volumenänderungen beeinflusst. Die Therapie mit einem kontinuierlichen positiven Atemwegsdruck (CPAP) führt neben einer Suppression der Apnoephasen zu einer Senkung der Vor- und Nachlast, was—insbesondere beim dilatierten Herzen—zu günstigen myokardialen Effekten führt.
Abstract
Obstructive sleep apnea (OSA) is common with an incidence of at least 500,000 patients in the German population. Typical symptoms are daytime sleepiness, headache in the morning, and snoring. Presumably obstructive sleep apnea via various mechanisms increases cardiovascular morbidity. Hypoxemia causes nocturnal hypertension in most of the patients. Nevertheless, about 20% of the patients develop daytime pulmonary hypertension and right heart dysfunction. Clinical and animal studies demonstrated right ventricular hypertrophy as a consequence of intermittent hypoxemia and pulmonary hypertension. Right ventricular hemodynamics differ essentially from left ventricular hemodynamics. Right ventricular function is substantially influenced by right ventricular afterload, which is mainly determined by pulmonary vascular resistance, and slightly influenced by preload. Application of continuous positive airway pressure (CPAP) via a nose mask normalizes nocturnal breathing disorders and reduces pre- and afterload, especially in patients with cardiomegaly. Therefore, CPAP generates positive effects on the myocardium.
Literatur
Alchanatis M, Tourkohoriti G, Kakouros S et al. (2001) Daytime pulmonary hypertension in patients with obstructive sleep apnea. The effect of continuous positive airway pressure on pulmonary hemodynamics. Respiration 68:566–572
Berman EJ, DiBenedetto RJ, Causey DE et al. (1991) Right ventricular hypertrophy detected by echocardiography in patients with newly diagnosed obstructive sleep apnea. Chest 100:347–350
Blankfield RP, Hudgel DW, Tapolyai AA, Zyzanski SJ (2000) Bilateral leg edema, obesity, pulmonary hypertension, and obstructive sleep apnea. Arch Intern Med 160:2357–2362
Bonsignore MR, Marrone O, Insalaco G, Bonsignore G (1994) The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms. Eur Respir J 7:786–805
Bonsignore MR, Marrone O, Romano S, Pieri D (1994) Time course of right ventricular stroke volume and output in obstructive sleep apneas. Am J Respir Crit Care Med 149:155–159
Bonsignore MR, Marrone O, Romano S (1992) Beat-by-beat analysis of pulmonary arterial pressure and flow during obstructive sleep apneas. Am Rev Respir Dis 145:721
Bradley TD, Rutherford R, Grossman RF et al. (1985) Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis 131:835–839
Buda AJ, Schroeder JS, Guilleminault C (1981) Abnormalities of pulmonary artery wedge pressures in sleep-induced apnea. Int J Cardiol 1:67–74
Budhiraja R, Tuder RM, Hassoun PM (2004) Endothelial dysfunction in pulmonary hypertension. Circulation 109:159–165
Chaouat A, Weitzenblum E, Krieger J et al. (1996) Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients. Chest 109:380–386
Deutsche Gesellschaft für Pneumologie (1991) Empfehlungen zur Diagnostik und Therapie nächtlicher Atmungs- und Kreislaufsregulationsstörungen. Pneumologie 45:45–48
Duchna H, Grote L, Sndreas S et al. (2003) Sleep disordered breathing and cardio- and cerebrovascular diseases: 2003 update of clinical significance and future perspectives. Somnologie 7:101–121
Fagan KA (2001) Physiological and genomic consequences of intermittent hypoxia: selected contribution: pulmonary hypertension in mice following intermittent hypoxia. J Appl Physiol 90:2502–2507
Guidry UC, Mendes LA, Evans JC et al. (2001) Echocardiographic features of the right heart in sleep-disordered breathing. The Framingham Heart Study. Am J Respir Crit Care Med 164:933–938
Hanly P, Sasson Z, Zuberi N, Alderson M (1992) Ventricular function in snorers and patients with onstructive sleep apnea. Chest 102:100–105
Krieger J, Sforza E, Apprill M et al. (1989) Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients. Chest 96:729–737
Laaban JP, Cassuto D, Orvoen-Frija E et al. (1998) Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity. Eur Respir J 11:20–27
Marrone O, Bellia V, Pieri D et al. (1992) Acute effects of oxygen administration on transmural pulmonary pressure in obstructive sleep apnea. Chest 101:1023–1027
Noda A, Okada T, Yasuma F et al. (1995) Cardiac hypertrophy in obstructive sleep apnea syndrome. Chest 197:1538–1544
Nolte D (2002) Woran stirbt ein Schlaf-Apnoe-Patient? Atemw Lungenkrkh 28:111–112
Permutt S, Bromberger-Barnea B, Bane HN (1962) Alveolar pressure, pulmonary venous pressure and the vascular waterfall. Med Thoracalis 19:239–260
Sajkov D, Cowie RJ, Thornton AT et al. (1994) Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome. Am J Respir Crit Care Med 149:416–422
Sajkov D, Wang T, Saunders N et al. (2002) Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea. Am J Respir Crit Care Med 165:152–158
Sanner B, Doberauer C, Konermann M et al. (1997) Pulmonary hypertension in patients with obstructive sleep apnea syndrome. Arch Intern Med 157:2483–2487
Sanner B, Konermann M, Müller HJ et al. (1995) Rechtsventrikuläre Funktion bei Patienten mit einer obstruktiven Schlafapnoe. Wien Med Wochenschr 145:518–520
Schäfer H, Hasper E, Ewig S et al. (1998) Pulmonary haemodynamics in obstructive sleep apnoea: time course and associated factors. Eur Respir J 12:679–684
Schulz R, Mahmoudi S, Hattar K et al. (2000) Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. Am J Respir Crit Care Med 162:570
Schulz R, Schmidt D, Blum A et al. (2000) Decreased plasma levels of nitric oxide derivates in obstructive sleep apnea: response to CPAP-Therapy. Thorax 55:1046–1051
Schulz R, Hummel C, Heinemann S et al. (2002) Serum levels of vascular endothelial growth factor are elevated in patients with obstructive sleep apnea and severe nighttime hypoxia. Am J Respir Crit Care Med 165:67–70
Siedl M, Schulz V (1997) Pulmonale Hypertonie bei Patienten mit obstruktivem Schlafapnoe-Syndrom. Atemw Lungenkrankh 23:523–529
Steiner S, Hennersdorf M, Schwalen A, Strauer B (2001) Right ventrcular performance in patients with sleep apnea and cardiovascular disease. Am J Respir Crit Care Med 163:400A
Thalhofer S, Kaufmann U, Dorow P (1991) Veränderung der Hämodynamik mit und ohne CPAP-Beatmung bei Patienten mit Schlafapnoesyndrom. Pneumologie 45:293–295
Tuder R, Groves B, Badesch D, Voelkel N (1992) Exuberantendothelial cell growth and elements of inflammation are present in plexiform lesions of pulmonary hypertension. Am J Pathol 144:275–285
Weitzenblum E, Krieger J, Apprill M et al. (1988) Daytime pulmonary hypertension in patients with sleep apnea syndrome. Am Rev Respir Dis 138:345–349
Yokoe T, Minoguchi K, Matsuo H et al. (2003) Elevated levels of C-reactive protein and interleukin-6 in patients with obstructive sleep apnea syndrome are decreased by nasal continuous positive airway pressure. Circulation 107:1129–1134
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Steiner, S., Strauer, B.E. Funktionelle Dynamik des rechten Ventrikels und des Lungenkreislaufes bei obstruktiver Schlafapnoe. Internist 45, 1101–1107 (2004). https://doi.org/10.1007/s00108-004-1266-8
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DOI: https://doi.org/10.1007/s00108-004-1266-8
Schlüsselwörter
- Obstruktive Schlafapnoe
- Rechter Ventrikel
- Pulmonalarterielle Hypertonie
- Cor pulmonale
- Kontinuierlicher positiver Atemwegsdruck (CPAP)