Schlaf und das Herz

Schlaf und das Herz

I. Auswirkungen des normalen Schlafes auf das Herz-Kreislauf-System
II. Schlafapnoe
III. Schlafapnoe und Herzinsuffizienz
IV. Schlafapnoe und Bluthochdruck
V. Schlafapnoe und Arrhythmien

GLOSSAR

Apnoe Beendigung des Luftstroms für mindestens 10 Sekunden.
Arrhythmie allgemeiner Begriff für eine Unregelmäßigkeit oder Schnelligkeit der
Herzschlag, ein abnormer Herzrhythmus.
Ausstoßfraktion der Bruchteil des aus dem Herzen ausgestoßenen Blutes
In die Arterien, in der Regel von 60 bis 75%; Eine niedrige
Ejektionsfraktion ist ein Marker der linksventrikulären Kontraktilität.
Herzinsuffizienz Versagen des Herzens, um ausreichend Blut aus
Die kammern in die aorta; Unzureichende Versorgung mit Blut
Erreicht Organe und Gewebe.
Hypopnoe abnorme Abnahme der Tiefe und Rate der Atmung.
Myokardinfarkt Tod einer Fläche von Herzmuskeln durch
Verstopfung einer Koronararterie durch Blutgerinnsel und Atherom;
Medizinischer Begriff für Herzinfarkt oder koronare Thrombose.

ES IST GUT EINGESCHLOSSEN, DASS DIESER KARDIAC-Tod am häufigsten innerhalb von wenigen Stunden nach dem Erwachen aus dem Schlaf auftritt. Erregung aus dem Schlaf

Verursacht zirkulierende, neuronale und hormonelle Veränderungen, die das Herz und das gesamte Kreislaufsystem beeinflussen; Der körper ist

Sofort für die Kampf- oder Fluchtreaktion vorbereitet. Es gibt erhöhte sympathische Aktivierung, erhöhte Sekretion von

Epinephrin (Adrenalin) und andere Prozesse, die zu einer Erhöhung der Herzfrequenz und des Blutdrucks führen. In Ergänzung,

Catecholamin-Sekretion induziert Thrombozytenpartikel im zirkulierenden Blut, um klebrig zu werden, was zu einem erhöhten Thrombozyten führt

Aggregation und Gerinnselbildung. Die Blockade des Blutflusses durch Thromben präzipitiert einen akuten Myokardinfarkt und plötzlich

Herztod Beta-adrenerge Blocker haben gezeigt, dass die frühe Morgen plötzliche Herztodrate um mehr als 35% zu reduzieren.

Die Erregung aus dem Schlaf hat daher tiefgreifende Einflüsse auf das Herz-Kreislauf-System. Kürzlich Schlafapnoe und die
Erregerreaktion hat gezeigt, dass sie eine Rolle bei der Erhöhung der Morbidität bei Patienten mit Herzinsuffizienz spielen.

Es muss jedoch betont werden, dass Schlafapnoe keine Herzinsuffizienz bei Personen mit normalem Herzen und normal verursachen

Ventrikuläre Funktion. Schlafapnoe sind nicht mit der Epidemie der Atherothrombose assoziiert, die die Hauptursache für das Herz ist

Angriff und Schlaganfall. Auch seine Verbindung mit der Verursachung der Bluthochdruck in der Bevölkerung insgesamt ist umstritten und ist

stark übertrieben. Jüngste Studien deuten darauf hin, dass Schlafapnoe mit einer erhöhten kardiovaskulären Morbidität assoziiert sind

I. EFFECTS OF NORMAL SLEEP ON THE CARDIOVASCULAR SYSTEM

Nonrapid eye movement (NREM) sleep comprises more than 85% of total sleep time and is associated with a state of cardiovascular
relaxation. There is a reduction in sympathetic nervous system activity, systemic arterial vascular resistance, heart rate, and
cardiac stroke volume.

Cardiac output ¼ cardiac stroke volume  heart rate: Blood pressure (BP) falls because of the decrease in cardiac
output (CO) and reduction in total peripheral resistance (TPR). BP ¼ CO  TPR: Vagal activity increases thus the heart rate falls
further to 40–60 beats per minute. Rapid eye movement sleep (REM) constitutes approximately
15% of total sleep time and intermittent surges in sympathetic discharge, heart rate, and blood pressure may
occur, but the average blood pressure and heart rate generally remain below waking levels.

II. SLEEP APNEAS

Obstructive sleep apnea (OSA) and central sleep apnea(CSA) are the two major recognized forms of sleep apnea.

Obstructive sleep apneas and hypopneas are caused by complete or partial collapse of an abnormally narrowed pharynx. In these
individuals the effort required to enhance airflow increases causing the rib cage and
abdomen to distort and move out of phase; thus, there is prominent respiratory effort. Central sleep apnea is caused by reductions
in the central respiratory drive manifested by an absence of respiratory effort.

A. Obstructive Sleep Apnea

Sleep apnea is defined as repetitive episodes of decreased or total cessation of repiratory airflow during sleep, leading
to a fall in oxygen saturation of 4% and sleep fragmentation. The severity of OSA is measured as the apnea-hypopnea index (AHI).
Approximately 20% of men and 10% of women in the North American population have an AHI greater than five events per hour of sleep.
By definition excessive daytime sleepiness must be present to be diagnostic for significant sleep apnea. Using this definition
only 4% of middle-aged men and 2% of women in North America manifest symptoms of OSA and an AHI of greater than five events per
hour of sleep. The diagnosis of sleep apnea is generally based on the demonstration of at least 10–15 apneas and hypopneas per
hour of sleep. This diagnosis is confirmed by the presence of excessive daytime sleepiness. Using this diagnostic claim less then
2% of the population is expected to have significant sleep apnea. Other symptoms include excessive snoring, restless sleep,
morning headaches, and fatigue, but these symptoms are nonspecific.

More than 96% of individuals that comprise the North American population have normal pharyngeal anatomy and sufficient partial
withdrawal of pharyngeal dilator muscle tone. This associated with pharyngeal collapse during sleep. It is not surprising,
therefore, that less than 2% of individuals without heart failure have significant OSA, a condition that is greatly exaggerated
and exploited.

Approximately 2% of North Americans have an anatomically narrowed pharynx and superimposition of the normal withdrawal of
pharyngeal dilator muscle tone during sleep, which causes the pharynx to constrict markedly restricting airflow and precipitating
apnea.

1. Mechanisms underlying the hypertensive effectsof OSA

These are multifactorial:

* Nocturnal chemoreflex activation by hypoxia and hypercapnia,
with consequent sympathetic activation causes
transient increase in blood pressure (see Figure 1).

* It has been postulated that the above effect might carry
over into excessive sympathetic activity and higher
blood pressure during daytime.

*Chemoreceptor resetting and tonic chemoreceptor
activation may probably contribute to daytime increases
in sympathetic activity and blood pressure.

2. Risk Factors for OSA

Obesity is a major risk factor of OSA. Obesity is present in approximately 70% of patients. It is the only major reversible risk
factor. The underlying mechanisms are unclear, however. Pharyngeal airway size is probably diminished with increased weight thus
increasing the propensity for obstructive apnea. It has been suggested that layering of fat adjacent to the pharynx narrows its
lumen in obese patients.

Alcohol consumption suppresses pharyngeal dilator muscle activation and may predispose individuals to obstructive apnea, but these
effects need further clarification and observation.

B. Central Sleep Apnea

Central sleep apnea that arises as a consequence of heart failure is known by physicians as Cheyne-Stokes respiration. It is a
manifestation of severe heart failure, New York Heart Association class IV. It is well recognized that patients who manifest
Cheyne-Stokes respiration have a poor prognosis and require aggressive medical therapy. Cheyne-Stokes respiration is a form of
periodic breathing during which CSAs and hypopneas alternate with periods of hyperventilation that have a waxing and waving
pattern of tidal volume. In CSA, arousals are not required for the initiation of airflow, but arousalsfrequently follow the
resumption of breathing.

Sleep is fragmented by frequent arousals but only a few patients complain of habitual snoring or excessive daytime sleepiness. The
administration of supplemental oxygen at night has been shown to abolish apnea-related hypoxia, but oxygen has not been shown to
cause improvement in cardiac function or quality of life over a one-month period.

III. SLEEP APNEA AND HEART FAILURE

Obstructive sleep apnea has been observed in 11% of patients with heart failure. The incidence of OSA in patients with heart
failure ranges from 11 to 37% as shown in data from small studies. Most important, Javaheri et al.

Noted that only a minority of patients in these studies complained of excessive daytime sleepiness, which suggests that many
patients with heart failure have relatively asymptomatic OSA. The mechanism by which heart failure increases the propensity to
precipitate OSA remains unclear, and its effects on morbidity and mortality in patients with heart failure require further
studies.
A randomized trial was done of patients with relatively severe OSA with an AHI of greater than 30 events per hour of sleep that
resulted in symptoms of excessive daytime sleepiness. This study showed that although patients randomized to CPAP (continuous
positive airway pressure) were compliant, they did not derive any symptomatic or neurocognitive benefit. These findings do not
support the use of CPAP for patients with OSA who have no complaint of excessive or inappropriate daytime sleepiness.

 

 

 

 

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