T. Podszus

Sleep apnea and pulmonary hypertension

SummaryThe pulmonary artery pressure values of 65 patients with sleep apnea syndrome were measured at rest and during ergometer exercise up to 100 W. Pulmonary hypertension at rest was found in 13, and during exercise in 31 more patients. Only 8 patients with pathological pressure findings suffered from pulmonary hypertension in combination with a pulmonary or cardiac disease. In the other 36 patients, no indication of a primary cause of pulmonary hypertension apart from sleep apnea syndrome could be found. Out of the 65 patients, 11 with a finding of more than 20 apnea episodes per hours sleep underwent polysomnographic recordings in the sleep laboratory. The hemodynamic parameters were continuously measured. All 11 patients had a finding of severe sleep apnea with more than 300 apnea episodes during the night of recording. In 6 patients, the appearance of apnea episodes was accompanied by only moderate changes in pulmonary artery pressure. In 5 patients, there were critical increases in pulmonary artery pressure, which went along with increases in cardiac output and in pulmonary capillary wedge pressure. Increases in pulmonary vascular resistance were established in 3 out of these 5 patients, and a slight decrease in 2. The mechanism of hypoxic vasoconstriction of the pulmonary arteries may account for the pressure increases in 3 of our patients, but fails to explain the findings in the other 2 patients. Nocturnal changes in pulmonary artery pressure in patients with sleep apnea may therefore have different causes. Pulmonary hypertension constitutes a severe complication in patients with sleep apnea. As 55% of all sleep apnea patients were found to suffer from pulmonary hypertension without any indication of a primary pulmonary or cardiac disease, the possibility that pulmonary hypertension results should not be underestimated in patients with suspected sleep apnea syndrome. Measurements of the pulmonary artery pressure must therefore be included in the examination regimen of such patients.

Sleep related disorders and internal diseases

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Nocturnal Hemodynamics in Patients with Sleep Apnea

Sleep apnea, a nocturnal disturbance of the respiratory regulation, has effects on the hemodynamics during sleep as well as during the day. The first systematic inquiries into these relationships were conducted as early as 1965 by Jung and Kuhlo [1]. In 1972, the research team of Coccagna and Lugaresi used direct measurements to document the blood pressure behavior during individual apnea episodes [2].

Prevalence of sleep apnea in healthy industrial workers

SummaryThe present study reports on polysomnographic findings of sleep apnea syndrome in a representative sample of otherwise healthy middle-aged blue collar workers (age 45.7±8.5) with normal to borderline blood pressure (systolic 135.5±16.1; diastolic: 88.3±10.2), mild overweight (Broca 114.9±14.7) and with reported nocturnal sleep disturbances. The prevalence of sleep apnea in this sample (N=20 out of a total of 78 workers with reported sleep disturbances) is 40%. Mean frequency of apnoeic episodes during night was 97.6±42.7 in the apnea-positive group as compared to 27.1±19.9 in the apnea-negative group (T=5.0;p<0.0001), with an apnea index of 13.3±6.2 as compared to 3.5±2.3 (T=7.2,p<0.0001). Left ventricular hypertrophy (mean diameter of end diastolic left ventricle: 64.0±9.5 mm) was found in individuals with apnea although manifest hypertension was absent in most individuals.

Intrathoracic pressure changes and cardiovascular effects induced by nCPAP and nBiPAP in sleep apnoea patients

SUMMARY  The effect of nasal continuous positive airway pressure (nCPAP) and nasal bi‐level positive airway pressure (nBiPAP) on intrathoracic pressure and haemodynamics during wakefulness was studied in a group of nine patients with severe sleep apnoea. No patient took cardiovascular medication.

Investigations of Arterial Baro- and Chemoreflexes in Patients with Arterial Hypertension and Obstructive Sleep Apnea Syndrome

Epidemiologic studies have shown that up to 10% of middle-aged men show more than ten cessations of breathing of more than 10s duration. In these patients an increase morbidity and mortality has been proved [17, 18]. Recently a striking association has been found between the occurrence of sleep apnea syndrome and essential hypertension [12, 27, 29, 33]. More than 50% of the patients with years of hypertension suffer from sleep apnea [39]. In humans a common mechanism included in the regulation of arterial blood pressure and ventilation is a reflex from arterial chemoreceptors [34, 35]. Carotid chemoreceptor reflex, activated by hypoxia, has been suggested to be involved in the pathophysiology of essential hypertension [42].

Electric stimulation of the upper airway muscle.

In various studies, it has been postulated that pharyngeal collapse occurring during sleep in obstructive sleep apnea may be alleviated by stimulating the genioglossus muscle. Basic experiments have demonstrated that neuromuscular stimulation applied intraorally via electrodes or by direct neural stimulation of the hypoglossal nerve might improve upper airway and respiratory function. An increase of maximal inspiratory airflow, an improvement of upper airway collapsibility and a decrease in respiratory events during sleep were observed. An impairment of sleep quality during electric stimulation has been excluded simultaneously. Considering clinical aspects, anatomical properties and long-term experience in electric stimulation it might be possible to develop full implantable devices as an alternative treatment for patients with obstructive sleep apnea.

WAS IST GESICHERT IN DER ANTIBIOTIKATHERAPIE ENTZUNDLICHER BRONCHOPULMONALERKRANKUNGEN

Zum ThemaUm bei der ätiologischen Vielfalt infektiöser Lungenparenchymerkrankungen eine rationale Diagnostik und Therapie zu ermöglichen, ist aufgrund epidemiologischer und klinischer Kriterien eine Einteilung in nosokomiale und ambulant erworbene Pneumonien sowie Pneumonien bei Immunsuppression sinnvoll. Die Festlegung der initialen kalkulierten Chemotherapie unter Berücksichtigung der Wahl einer Mono- oder Kombinationstherapie muß sich nach Kriterien wie Schweregrad der Infektion, Alter, Morbidität und Risikofaktoren sowie dem Zeitpunkt der Manifestation der Erkrankung richten.Nur durch die zielgerichtete Wahl des initialen Antibiotikums können die klinische Effektivität gesichert und unnötige Folgekosten, die heutzutage aufgrund der geringeren finanziellen Ressourcen im Gesundheitssystem mehr denn je zu berücksichtigen sind, vermieden werden. Eine insuffiziente antibiotische Initialtherapie erhöht nicht nur die Gesamtbehandlungskosten durch verlängerte Therapiedauer, sie bedingt auch eine erhöhte Letalität von Patienten mit schweren Pneumonien.

Pathogenese der schlafbezogenen Atmungsstörungen

Epidemiologische Studien der letzten Jahre belegen fur die schlafbezogenen Atmungstorungen (SBAS) eine hohe Pravalenz [21]. So sind mehr als zwanzig Prozent der Manner Schnarcher [17]. Weiterhin wird allein fur den intermittierenden nachtlichen Atemstillstand, die sog. Schlafapnoe, bei Mannern der mittleren Altersgruppe eine Pravalenz von bis zu zehn Prozent angenommen [14, 19]. Eine hohe Koinzidenz der Schlafapnoe und des lauten und unregelmasigen Schnarchens mit einer erhohten Morbiditat — vor allem bezuglich kardiovaskularer und kardiopulmonaler Erkrankungen [24] — ist ebenso nachgewiesen wie eine erhohte Invaliditat und Mortalitat [15, 20, 28]. Bei der Pathogenese der schlafbezogenen Atmungsstorungen spielen zirkadiane Mechnismen eine eher untergeordnete Rolle, die entscheidende pathogenetische Rolle kommt dem Schlaf selbst zu. Daher ist der hier benutzte Begriff „schlafbezogene Atmungsstorungen“dem der „nachtlichen Atmungsstorungen“vorzuziehen.

Assessment of the Time Structure of Sleep Apneas

The apnea index serves as a quantitative indication of the seriousness of the disorder [1]. It makes use of the total number of apneic episodes per hour without respect to their duration. However, frequent, long-lasting episodes may lead to a threatening drop in oxygen saturation, eventhough the apnea index will show reduced values. An additional assessment of each apnea length, separated into central, obstructive, or mixed apnea seems invaluable in the differential diagnosis of the pathogenetic components contributing to the sleep apnea syndrome. We therefore developed an automatic procedure which enables, with high accuracy, a computerized evaluation of apnea length.