PRODUKTKATALOG
Wir unterstützen Sie
zu Hause
in der Praxis
in der Klinik
TNI medical AG
Hofmannstr. 8
D-97084 Würzburg
Tel.
Fax
+49 931 20 79 29-02
+49 931 20 79 29-01
E-Mail:
Internet:
[email protected]
www.tni-medical.de
ARTIKELNUMMER: 30200040 VERSION 1.2
Therapie
Vorwort
Diagnose
Liebe Partner und Kunden,
die Medizintechnik gehört zu den größten Wachstumsmärkten weltweit. Mit Innovationszyklen, die im Durchschnitt kleiner als 5 Jahre sind, geht die Entwicklung in der
Medizintechnik noch vor der Automobilbranche mit rasantem Tempo voran.
Unsere Branche ist geprägt vom intensiven Austausch der medizinischen Forschung
mit technologischen Disziplinen und daraus folgender Anwendungsentwicklung.
Die gewonnenen Erkenntnisse werden schnell und zielgerichtet in neue Produkte
umgesetzt. TNI medical AG ist ein Vorreiter in der Entwicklung neuer Technologien
für die Atmungsunterstützung. Wir haben uns dabei der Maximierung des Patientenkomforts bei gleichzeitiger Einhaltung der Kosteneffizienz verschrieben. Unsere
Produktneuheit TNI® (Therapie mit nasaler Insufflation – Applikation von warmer und
befeuchteter Luft bzw. Luft/Sauerstoffgemische mit hohen Flussraten in die Nase)
setzt dabei am wichtigsten Punkt an: der Schnittstelle zum Patienten.
Im Austausch mit Medizinern, Patienten und Verbänden ist es unsere Aufgabe, die
Entwicklung, die Herstellung und den flächendeckenden, zuverlässigen Vertrieb und
Service von Diagnose- und Beatmungsgeräten kontinuierlich voranzutreiben und zu
verbessern.
In diesem Katalog finden Sie unser Angebot an hochwertigen Geräten und Zubehör. Unsere Produkte zielen auf einen maximalen Patientenkomfort und den damit
verbundenen Therapieerfolg. Daneben liegt unser Fokus auf einer intuitiven Bedienbarkeit, so dass die Produkte im Alltag des medizinischen Fachpersonals und beim
Patienten zu Hause kostengünstig und sicher einsetzbar sind. Wir sind uns dabei
unserer Verantwortung gegenüber den Patienten, den Ärzten und dem Klinikpersonal bewusst und pflegen ein aufwändiges, lückenloses Qualitätsmanagementsystem
nach neusten Anforderungen.
Neuste Erkenntnisse aus der Forschung an mehreren Zentren in Europa und den USA
flossen unmittelbar in die Entwicklung dieser High-Flow Luft- und Sauerstoffbeatmung ein und finden sich in der TNI® Produktfamilie wieder. Die aktuellen Ergebnisse
aus der klinischen Forschung sowie daraus resultierende mögliche Anwendungsbereiche sind ebenfalls in diesem Katalog für Sie zusammengefasst.
Eine perfekte Dienstleistung und ein hervorragender Service setzen für uns die enge
und reibungslose Zusammenarbeit zwischen Ärzten, Klinikpersonal, Patienten und
Lieferanten medizintechnischer Geräte voraus - zum Wohle der Patientinnen und
der Patienten.
Ewald Anger
Vorstand TNI medical AG
2
Therapie
Diagnose
Inhalt
Produktübersicht
...................................................................................................
4
Geräteübersicht
...................................................................................................
Artikelnummern
............................................................................
Anwendungsbereiche ............................................................................
6
5
8
Produkte
...............................................................................................................
®
TNI Produkte ...................................................................................................
TNI®20 ...................................................................................................
................................................................
TNI®20s oxy (Klinik)
................................................................
TNI®20 oxy (Homecare)
9
9
9
9
10
CPAP Produkte
.......................................................................................
iSleep 20 i, iSleep 20+
................................................................
ISleep 22, iSleep 25
................................................................
12
12
13
Diagnoseprodukt
MS310
Embletta Gold
Embla S4500
Embla N7000
14
14
16
17
18
.......................................................................................
.......................................................................................
........................................................................................
........................................................................................
.........................................................................................
TNI® Wirkungsweise ...................................................................................................
Resultate aus Studien und Tests
....................................................
®
....................................................
TNI Wirkungsweise bei COPD
19
21
24
TNI® Studien
...............................................................................................................
25
Fallbeispiele ...............................................................................................................
Erwachsene ...................................................................................................
TNI®20 ...................................................................................................
................................................................
TNI®20 oxy / TNI®20s oxy
Kinder ...............................................................................................................
TNI®20 ...................................................................................................
60
60
60
61
65
65
Über uns
...............................................................................................................
Kontaktdaten ...................................................................................................
66
66
Kontaktformular
67
....................................................................................................
3
Therapie
Diagnose
Produktübersicht
Therapie
TNI®20
führt dem Patienten einen warmen, befeuchteten Raumluftstrom von maximal 20 Litern Luft pro Minute über einen speziellen, lautstärkeoptimierten Applikator
(Nasenbrille) in die Nase.
TNI®20 oxy kombiniert die Vorteile der SauerstofftheraO2
pie und der High-Flow Beatmung für die Versorgung in der
häuslichen Umgebung.
TNI®20s oxy ein Luftbefeuchter für die Klinikdruckluft,
kombiniert Sauerstofftherapie und High-Flow Beatmung.
Als Zubehör dient der fahrbare Infusionsständer inkl.
Halterung für die Befeuchter- und Anschlusseinheit.
iSleep 20+/iSleep 20i/iSleep 22/iSleep 25
werden zur Behandlung nächtlicher Schlafapnoen eingesetzt.
Der Atemluftbefeuchter HA 20 kann optional an die CPAP/
Bilevel-Geräte angebracht werden.
4
Therapie
Diagnose
Diagnose
MS310 Polygraphiesystem für die portable Diagnose- und
Therapiekontrolle der schlafbezogenen Atmungsstörungen,
inklusive Auswertesoftware und Praxiskopplung über GDTSchnittstelle.
Embletta Gold Polygraphiesystem für die ambulante
Schlafuntersuchung, inklusive RIP-Technologie und Auswertesoftware.
Embla S4500 Polysomnographiesystem für die robuste
und zuverlässige kardiorespiratorische Schlafuntersuchung.
Embla N7000
Polysomnographiesystem für die robuste und zuverlässige kardiorespiratorische und neurologische
Schlafuntersuchung
5
Therapie
Geräteübersicht
Diagnose
Artikelnummern
Gerät und Beschreibung
405 00001
TNI®20 - High Flow Beatmung durch Therapie mit nasaler Insufflation (TNI®)
Das TNI®20 System liefert einen Raumluftstrom, der erwärmt und befeuchtet ist. Dieser
wird dem Patienten durch einen speziellen, lautstärkeoptimierten und beheizten Applikator (Nasenbrille) verabreicht. Das System kann einen Gesamtfluss von bis zu 20 Liter pro
Minute liefern, individuell nach Verordnung regelbar.
405 00002
TNI®20s oxy - High Flow Beatmung durch Therapie mit nasaler Insufflation (TNI®)
Das TNI®20s oxy Gerät appliziert dem Patienten ein warmes befeuchtetes Luft-Sauerstoffgemisch von maximal 20 Liter Luft pro Minute. Dieses wird dem Patienten durch einen
speziellen, lautstärkeoptimierten und beheizten Applikator (Nasenbrille) verabreicht.
Das Luft-Sauerstoffgemisch wird aus den klinikseitig vorhandenen Wandanschlüssen bezogen, individuell nach Verordnung regelbar.
405 00003
TNI®20 oxy - High Flow Beatmung durch Therapie mit nasaler Insufflation (TNI®)
Das TNI®20 oxy System liefert einen Gesamtfluss, bestehend aus Raumluft und Sauerstoff
welcher erwärmt und befeuchtet ist. Dieser wird dem Patienten durch einen speziellen,
lautstärkeoptimierten und beheizten Applikator (Nasenbrille) verabreicht.
Dem durch das TNI®20 oxy System generierten Luftstrom kann individuell Sauerstoff bis
zu 8 Liter pro Minute beigemischt werden, aus gebräuchlichen Quellen wie einem Sauerstoffkonzentrator oder Flaschen mit Flüssigsauerstoff entnommen. Das System kann einen
Gesamtfluss von bis zu 20 Liter pro Minute liefern, individuell nach Verordnung regelbar.
402 00050
iSleep 20 i
Das iSleep 20 i ist ein fortschrittliches, automatisch den Therapiedruck anpassendes CPAPGerät.
402 00051
iSleep 20 +
Das iSleep 20 + ist ein hochwertiges CPAP-Gerät, entwickelt für die Anwendung zu Hause.
402 00015
iSleep 22
Das iSleep 22 ist ein BI-LEVEL S-Gerät, entwickelt für die Anwendung zu Hause.
402 00014
iSleep 25
Das iSleep 25 ist ein BI-LEVEL ST-Gerät, entwickelt für schlafbezogenen Atemstörungen.
THERAPIE
6
Art. Nr.
Therapie
Geräteübersicht
Diagnose
Artikelnummern
Gerät und Beschreibung
9A00002
MS310
Polygraphiesystem für die portable Diagnose- und Therapiekontrolle der schlafbezogenen
Atmungsstörungen, inklusive Auswertesoftware und Praxiskopplung über GDT-Schnittstelle.
404 00550
Embletta Gold
Polygraphiesystem für die ambulante Schlafuntersuchung, inklusive RIP-Technologie und
Auswertesoftware.
405 00501
Embla PSG S4500
Polysomnographiesystem für die robuste und zuverlässige kardiorespiratorische Schlafuntersuchung.
404 00500
Embla PSG N7000
Polysomnographiesystem für die robuste und zuverlässige kardiorespiratorische und neurologische Schlafuntersuchung.
DIAGNOSE
Art. Nr.
7
Therapie
Diagnose
Geräteübersicht
Anwendungsbereiche
TNI® THERAPIE
TNI®20
TNI Therapie Anwendungsbereiche
TNI®20 oxy
TNI®20s oxy
5 bis 20
5 bis 25
0 bis 8
0 bis 16
Erwachsene:
OSA mit leichter bis mittelschwerer Ausprägung
UARS
Overlap Syndrom
COPD Stadium I
COPD Stadium II
COPD Stadium II und III mit Partial-Insuffizienz
COPD Stadium III und IV mit Global-Insuffizienz
Fibrose
Nach Lungen-Teilresektion und Transplantation
Kinder und Jugendliche (sehr große Effektivität und Therapieakzeptanz):
Bei Strömungsbehinderung
OSA und OSA Symptome
Gesichtsfehlbildungen mit spez. Gesichtsanatomien
Down-Syndrom
Frühgeborene und Kleinkinder:
Pulmonale Dysplasie mit Sauerstoffbedarf
Chronisch respiratorische Insuffizienz
Alternative bei nicht durchführbarer Heim CPAP-Therapie
Homecare Anwendungen
TNI Therapie Allgemeines
Einstellungen:
Gesamtfluss (L/min)
5 bis 20
O2 (L/min)
Anzeige Ist-Flow
Technische Daten:
Medizinprodukteklasse (93/42/EWG)
Schallabstrahlung
< 32 dB (A)
< 32 dB (A)
Betriebsspannung
100-240 V AC
100-240 V AC
100-240 V AC
50-60 Hz
50-60 Hz
50-60 Hz
25/21/23,5
26/21/23,5
< 8,5
< 8,5
26/22/10
26/22/10
26/22/10
< 2,0
< 2,5
< 3,0
1,8
1,8
1,8
Lüftereinheit (Kompressoreinheit):
Abmessung L/B/H (cm)
Gewicht (kg)
Befeuchtereinheit:
Abmessung L/B/H (cm)
Gewicht (ohne Wasser) (kg)
Applikator:
TNI Applikator für Erwachsene (Standard)
TNI Applikator für Erwachsene (Komfort)
TNI Pediatric Applikator
TNI Pediatric Adapter
TNI Paed Adapter (BC 2745, BC 2755)
Schlauchlänge (m)
Legende:
8
ja
eingeschränkt
nein
Therapie
Diagnose
Produkte
TNI® Produkte
TNI® - Therapie mit nasaler Insufflation
Methode
TNI® (Therapie mit nasaler Insufflation) ist eine weltweit neue Methode zur Atmungsunterstützung. Sie arbeitet
nicht mit Überdruck, sondern ist eine High-Flow-Beatmungsmethode, wobei ein konstanter warmer und feuchter Luftstrom durch eine dünne Nasenbrille in die Nase des Patienten appliziert wird und zu einer Verbesserung
der Ventilation führt. Diese Methode bietet einen hohen Komfort für den Patient. Im Gegensatz zu den bereits
seit mehreren Jahren erhältlichen nasalen „Prongs“-Masken bleibt die Nase bei TNI® offen, d.h. die Enden des
Applikators verschließen die Nase nicht.
TNI®20
Indikationen
Im Bereich Heimbeatmung werden mit dem Therapiegerät TNI®20 schlafbezogene Atmungsstörungen behandelt. Bei Patienten mit einem vergleichbaren CPAP Druck bis ca. 8 mBar zeigt die Methode eine gute Effektivität1.
Zusätzlich wurde TNI® bereits erfolgreich als Ersatztherapie bei Patienten mit schwerer Symptomatik, die CPAP
nicht tolerieren, eingesetzt.
VORTEILE:
•
•
•
•
•
•
•
•
Mit TNI® ist die Bauchlage während des
Schlafs möglich
•
•
Hoher Tragekomfort, einfache Bedienung
Keine Nebenwirkungen durch eine Maske
(wie z. B. Drucknekrosen, Bindehautentzündungen)
Ständige Kommunikationsmöglichkeit (kein Absetzen der
Maske nötig)
Entlastung der Atemanstrengung
Patient wird nur minimal in seiner Mobilität eingeschränkt.
Keine Aspirationsgefahr durch Erbrechen
Keine Unterbrechung der Beatmung beim Abhusten
von Bronchialsekret
Kein Austrocknen von Mund und Nase
Keine Druckeinstellung oder individuelle Anpassung nötig
Lieferumfang:
→
Lüftereinheit
•
→
•
•
Befeuchtereinheit
•
•
steht in Bettnähe
typisch auf dem
Nachttisch
wird vom Patienten entfernt
platziert
steht in Bodenhöhe
Entfernung im Radius max. 5
Meter
→
- 1 Lüftereinheit
- 1 Befeuchtereinheit
- 1 Applikator für Erwachsene
- 1 Verbindungsschlauch
- 1 Verbindungskabel
- 1 Netzanschlussleitung
- 1 Gebrauchsanweisung
für den Patienten
- 2 Bestellformulare
- 1 Kurzanleitung
- 1 Patientenpass
- 1 Rückumschlag
Applikator
•
•
•
bildet die Schnittstelle zum Patienten
hat die Optik einer Nasenbrille
Besteht aus weichem Material mit
angenehmem Tragekomfort
1 Nilius G et al (2007): “Multicenterstudie zur Wirksamkeit der transnasalen Insufflation (TNI®) bei leichter bis mittelgradiger pharyngealer
Obstruktion und Schlafapnoe”, Somnologie 11, Supplement 1:26 [conference abstract]
9
Therapie
Diagnose
Produkte
TNI®20s oxy (Klinik) &
TNI®20 oxy (Homecare)
Indikationen
Mit TNI®20s oxy und TNI®20 oxy existiert eine neue, sehr einfach anzuwendende Therapiemöglichkeit zur Behandlung respiratorischer Insuffizienz, welche die Lücke zwischen einer einfachen Sauerstofftherapie mit niedrigen Flüssen und der nicht-invasiven Beatmung füllt. Die Therapie ist sehr einfach anwendbar und für den Patienten wegen der Erwärmung und Befeuchtung des Luft/Sauerstoffflusses und des geringen Einflusses auf seine
Spontanatmung deutlich angenehmer als vergleichbare Therapieformen.
•
•
Anschlusseinheit
Befeuchtereinheit
→
•
•
•
•
COPD
Respiratorische Insuffizienz
post-operative Atmungsunterstützung
prophylaktische Anwendung nach herzchirurgischen Eingriffen
Atmungsunterstützung nach einer Extubation
Atmungsunterstützung nach der Anästhesie
Atmungsunterstützung nach einem Schlaganfall
Erkrankungen mit schwerer chronischer Hypoxämie (z.B. pulmonale Hypertonie)
Rehabilitation bei Lungererkrankungen
Entwöhnung nach Beatmung (Weaning)
→
•
•
•
•
KLINIK
→
Möglichkeiten der klinischen Anwendung:
Applikator
Atmungsunterstützung zu Hause mit dem TNI®20 oxy
TNI®20s oxy ist auch als preisgünstige Version für den Einsatz in der Homecare erhältlich, mit einer angenehm
leisen und zuverlässigen Luftquelle, die ursprünglich für die Schlafmedizinversion des Gerätes, das TNI®20, entwickelt wurde. Es kann Druckluft aus der mobilen Luftquelle mit Sauerstoff aus gebräuchlichen Quellen wie einem
Sauerstoffkonzentrator oder Flaschen mit Flüssigsauerstoff kombinieren.
→
10
Applikator
→
→
• Atmungsunterstützung bei respiratorischer
Insuffizienz
• Overlap syndrom
• Lungenfibrose
• Mukoviszidose
• Asthma Attacken, vor allem im Zusammenhang
mit kalter Luft oder Entzündung der Atemwege
• Rhinitis oder Sinusitis
• Kongestive Herzinsuffizienz
O2
• Neuromuskuläre- und Thoraxwanderkrankungen
(z.B. Amyotrophe Lateralsklerose (ASL), Muskeldystrophie Duchenne (DMD), spinalen Muskel
atrophie (SMA), Post-Polio-Syndrom, Post-Tuber
kulose-Syndrom)
Sauerstoffquelle
→
Befeuchtereinheit
Lüftereinheit
HOMECARE
Mögliche Einsatzgebiete in der Homecare:
Therapie
Diagnose
Produkte
VORTEILE:
Patienten können durch die Homecare-Variante TNI®20 oxy früher wieder in ihr soziales Umfeld zu Hause eingegliedert werden, ohne auf die Atmungsunterstützung verzichten zu müssen oder komplizierte
und teure Betreuung zu organisieren.
•
•
•
•
•
•
•
•
•
•
•
Entlastung der Atemanstrengung
Keine Aspirationsgefahr durch Erbrechen
Wärmt und befeuchtet den beigemischten Sauerstoff, dadurch kein Austrocknen von Mund und Nase
Verbessert das Abhusten durch die feuchte und warme Luft
Keine Unterbrechung der Beatmung beim Abhusten von Bronchialsekret
Keine Druckeinstellung oder individuelle Anpassung nötig
Verwirbelt das Luft-O2-Gemisch im Totraumvolumen
Erhöht dadurch die Ventilation und sorgt für eine CO2-Auswaschung.
Verbessert die Atemeffizienz: (VD/VT) und damit die Belüftung der Lunge (VA)
Reichert das VD mit „brauchbarem“ Luft-O2-Gemisch an
Vermindert den arteriellen CO2 Gehalt durch die Verbesserung der VA. (Mit Verabreichung von nur
reinem Sauertoff nicht erreichbar.)
Lieferumfang TNI®20 oxy:
Lieferumfang TNI®20s oxy:
- 1 Lüftereinheit mit Ventil zur Sauerstoffbeimischung
(techn. Rückflussreduzierventil)
- 1 Befeuchtereinheit
- 1 Applikator für Erwachsene
- 1 Verbindungsschlauch
- 1 Verbindungskabel
- 1 Netzanschlussleitung
- 1 Sauerstoff- und Sicherheitsschlauch
- 1 Gebrauchsanweisung
- 1 Mischtabelle
- 1 Patientenpass
- 1 Befeuchtereinheit
- 1 Anschlusseinheit
- 1 Applikator für Erwachsene
- 1 Verbindungsschlauch
- 1 Netzanschlussleitung
- 1 Gebrauchsanweisung
- 1 Kurzanleitung mit Mischtabelle
- 1 Sensorkabel
als Zubehör dient der
TNI® Gerätewagen
als Zubehör dient der
Infusionsständer für das TNI®20s oxy
Halterung
Anschlusseinheit
Halterung
Befeuchtereinheit
→
→
→
Korb
Halterung
Lüftereinheit
→
→
→
Fahrbarer Gerätewagen inklusive der Halterung
für die Befeuchter- und Lüftereinheit sowie Korb.
Fahrbarer Infusionsständer inklusive der Halterung für
die Befeuchter- und Anschlusseinheit sowie Korb.
11
Therapie
Produkte
Diagnose
CPAP Produkte
Methode
Kontinuierliche positive Überdruckbeatmung, CPAP abgekürzt. Dabei wird bei dem Patienten ein kontinuierlicher, hoher Überdruck über eine Nasen- oder Gesichtsmaske in den oberen Atemwegen aufgebaut.
iSleep 20i, 20+
Das iSleep 20i ist ein fortschrittliches, automatisch den Therapiedruck anpassendes CPAPGerät.
•
•
•
•
•
•
•
•
•
•
Erweitertes und dennoch leicht ver
ständliches Bedienfeld
mit großen Tasten
Grosses grafisches Display mit Hintergrundbeleuchtung
Integrieter Wecker
Rückseitiger Schlauchanschluss
Automatischer Start nach kurzem
Stromausfall
Flexible Spannunsversorgung für den
mobilen Patienten
Kompatibel zu einer Vielzahl von Masken
Einzigartige Snooze-Funktion
Detaillierter Patientenspeicher mit optionaler Speicherkarte (CF)
Integrierter AHI und Leckagekalkulation
Lieferumfang
- Tasche
- Netzkabel
- Netzteil
- Schlauch
- Ersatzfeinfilter
- Gebrauchsanweisung
- Patientenkurzanleitung
Das iSleep 20+ ist ein hochwertiges CPAP-Gerät,
entwickelt für die Anwendung zu Hause. Dank
der einzigartigen eAdapt-Technologie wurde der
Therapiekomfort wesentlich erhöht.
•
•
•
•
•
•
•
•
•
•
eAdapt für höchsten Anwenderkomfort
Erweitertes und dennoch leicht verständliches Bedienfeld mit großen Tasten
Grosses grafisches Display mit Hintergrundbeleuchtung
Integrierter Wecker
Rückseitiger Schlauchanschluss
Flexible Spannungsversorgung für den
mobilen Patienten
Kompatibel zu einer Vielzahl von Masken
Einzigartige Snooze-Funktion
Detaillierter Patientenspeicher mit optionaler Speicherkarte (CF)
Integrierter AHI und Leckagekalkulation
Warmluftbefeuchter HA 20
•
•
•
•
•
12
Vollständig integrierbar
Permanente Überwachung des Wasserspiegels durch den transparenten
Wasserbehälter
Optionale Befeuchtung
Individuell einstellbare Befeuchterleistung in 9 Stufen
Einfach zu befüllen und leicht zu reinigen
Therapie
Diagnose
CPAP Produkte
Methode
Kontinuierliche positive Überdruckbeatmung, Bi-LEVEL abgekürzt. Dabei wird bei dem Patienten ein kontinuierlicher, hoher Überdruck über eine Nasen- oder Gesichtsmaske in den oberen Atemwegen aufgebaut.
iSleep 22, 25
Das iSleep 22 ist ein BI-LEVEL S-Gerät.
•
•
•
•
•
•
•
eSync, synchrone Atemzugstriggerung
Einstellbarer Inspirationstrigger
Automatisch Leckage-kompensierter
Exspirationstrigger
Fixe Backup-Frequenz
Integrierter Wecker
Optionale Speicherkarte
Integrierte Leckagekalkulation
Das iSleep 25 ist ein BI-LEVEL ST-Gerät
Lieferumfang
•
•
•
•
- Tasche
- Netzkabel
- Netzteil
- Schlauch
- Ersatzfeinfilter
- Gebrauchsanweisung
- Patientenkurzanleitung
•
•
•
eSync, synchrone Atemzugstriggerung
Einstellbare Trigger (Inspiration und Exspiration)
Einstellbare Backup-Frequenz und Anstiegszeit
Detaillierter Patientenspeicher mit Druck, Flow,
Leckage, Frequenz und Tidalvolumen
Integrieter Wecker
Optionale Speicherkarte
Integriete Leckagekalkulation
Warmluftbefeuchter HA 20
•
•
•
•
•
Vollständig integrierbar
Permanente Überwachung des Wasserspiegels durch den transparenten
Wasserbehälter
Optionale Befeuchtung
Individuell einstellbare Befeuchterleistung in 9 Stufen
Einfach zu befüllen und leicht zu reinigen
13
Therapie
Diagnose
Produkte
Diagnoseprodukt
MS310 - portables Screening für schlafbezogene Störungen
MS310 ist ein Medizinprodukt zur Aufzeichnung und Diagnostik von schlafbezogenen Störungen in der gewohnten Umgebung des Patienten, insbesondere zur Erkennung und Analyse von Apnoen und Hypopnoen, Entsättigungen, Schnarchgeräuschen, Atemfrequenz, Schnarchfrequenz und Pulsfrequenzänderungen. Außerdem kann
das MS310 auch zur CPAP - Therapiekontrolle eingesetzt werden.
Aufgezeichnet werden können:
• Atemfluss mit einem Thermistor (nasal/oral) oder einer Nasenbrille (Drucksignal)
• Atemantrieb (Thorax und Abdomen) mit piezoelektrischen Dehnungssensoren
(2 Piezosensoren pro Sensor für optimale Signalqualität)
• Sauerstoffsättigung (SpO2) und Pulsfrequenz (inkl. Pulswellenkurve) mit
einem Fingerclip (integriertes Pulsoximeter)
• Körperlage (Rücken, Bauch, Links, Rechts, Stehend) mit dem integrierten
Lagesensor
• Schnarchengeräusche, gemessen mit dem integrierten Mikrofon
• Schnarchfrequenz, Schnarchpegel, gemessen mit dem integrierten Mikrofon
• nCPAP/BiLevel Druck
• CPAP/BiLevel- Atmung
• Erweiterungsanschluss (Extension-Bus, AUX) steht für weitere Sensoren zur
Verfügung
Die Sensoren wurden speziell für den ambulanten Einsatz
entwickelt und zeichnen sich durch einfache Handhabung
aus. Das Design des MS310 Polygraph ist kompakt und
benutzerfreundlich.
Mit der MS300 Software lassen sich individuelle Reports
erstellen. Auf einfachste Weise lassen sich Analyseergebnisse in Form von Farbgraphiken, Wertetabellen und freien
Textfeldern zusammenstellen und für den ausgewählten
Patienten ausdrucken.
Durch die GDT Schnittstelle können Messergebnisse an die
Praxissoftware weitergeben werden. Von der Praxissoftware aus kann ein beliebiger Patient in der MS300 Software aufgerufen und dessen Ergebnisse auch graphisch
dargestellt werden.
14
Therapie
Diagnose
Produkte
Umfangreiche Optionen
3 PLM Option
3 EKG Option
9 Versichertenkartenlesegerät
3 Softfingerclip
VORTEILE:
•
•
•
•
•
•
•
•
•
Robuste und einfach anzulegende Sensoren
Hoher Tragekomfort (integrierte Sensoren)
Schnelle und sichere Diagnostik
Automatische und manuelle Analyse
Einfache Bedienung
Abrechnungsfähigkeit nach EBM (30900)
Niedrige Betriebskosten
GDT Schnittstelle zur Praxissoftware-Anbindung
EKG- / PLM Option (IGEL Leistung)
GDT Schnittstelle (Standard 2.1)
1. Kommando:
(Satzart 6302)
Neue Untersuchung über die Praxis-EDV an die MS310 Software anfordern
2. Kommando: Übermitteln der wichtigsten Untersuchungsergebnisse (Index) an die Praxis-EDV
(Satzart 6310)
3. Kommando: Messdaten (Rohdaten) über die Praxis-EDV anfordern und Untersuchungsergebnisse
(Satzart 6311) anzeigen lassen
Lieferumfang:
-1 MS310 Rekorder
-1 Sauerstoffsättigungssensor
-1 Nasensensor (Thermistor nasal/oral)
-1 Trageteller mit Thoraxsensor und
Schnarchmikrophon
-1 Abdomensensor
-2 Tragebänder 1,50m (an der
Innenseite farblich markiert)
-2 Tragebänder 1,10m
-1 Nackengurt
-2 Armbänder
-1 CPAP Drucksensor, komplett
-1 T-Verbindung mit Verbindungsschlauch CPAP
-1 USB Kabel
-2 Batterien, 1,5 V Mignon
-1 Desinfektionsmittel
-1 Fixierpflaster
-1 CD MS300 Windows Software
-1 Gebrauchsanweisung
-1 Kurzanleitung für den Patienten
-1 Tragekoffer
und
tasche
n
e
t
n
e
i
t
inkl. Pa u-Ladegerät
Akk
15
Therapie
Diagnose
Diagnoseprodukt
Embletta Gold - tragbares Diagnosegerät
Das Embletta Gold ist ein flexibles, kompaktes und optimiertes Aufzeichnungsgerät, das leicht zu handhaben ist.
Durch ihre Robustheit eignet sich die Embletta Gold sowohl für das klinische Umfeld, als auch für den Gebrauch
im häuslichen Umfeld - ohne Beeinträchtigung der einwandfreien Qualität und der Leistungsstärke, die für das
Fachpersonal in der Schlafmedizin inzwischen selbstverständlich geworden sind.
Aufgezeichnet werden können:
•
•
•
•
•
•
•
Atemflussstaudruck (Nasenkanüle)
Oraler Atemfluss
Maskendruck
XFlow* (von XactTrace-Gurten mit RIP-Technologie)
Schnarchen (von Nasenkanüle)
Differenzdruck
Abdominale Bewegung
(von XactTrace-Gurten mit RIP-Technologie)
Thoraxbewegung
(von XactTrace-Gurten mit RIP-Technologie)
Sp02 Mittelwert (Oximeter)
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Sp02 Beat-to-Beat (Oximeter)
Pulsfrequenz (Oximeter)
Pulswelle (Oximeter)
Körperlage
Bewegung
Ereignismarkierung
EKG
EEG
EOG
AUX-Eingang (Gleichstrom)
(0 – 1 Volt)
Online-Aufzeichnung
AutoSet-Schnittstelle
*Zusätzliches Atemflusssignal als zuverlässiger Ausfallschutz bei Untersuchungen ohne Atemflusssensoren
Überragendes Konzept
Flexibel
•
•
•
16
Schnittstelle für externe Geräte,
z. B. zur PtCO2- Überwachung
Aufzeichnung des Atemflusssignals
mit gängigen Flussgeneratoren oder
Beatmungsgeräten
Geeignet für ambulante und stationäre
Aufzeichnungen
Präzise
•
•
•
Benutzerfreundlich
•
•
•
•
•
Praktische wiederaufladbare Batterien
Leicht und robust
Farbcodierte Anschlüsse erleichtern
das Anlegen der Sensoren
•
Präziser und schneller Druckmesswandler
zur Evaluierung von Atemfluss und
Atemflusslimitation
Hervorragende Qualität des
Atemanstrengungssignals vom
XactTrace-Gurt dank RIPTechnologie (respiratorische
Induktionsplethysmographie)
Höchste Genauigkeit bei
Titrationsuntersuchungen mit
Geräten beliebiger Hersteller
Zusätzliches Atemflusssignal von XFlowTM
als zuverlässiger Ausfallschutz bei
Untersuchungen ohne Atemflusssensoren
Eingebauter Aktometer und
3D-Körperlagesensor
Automatische Plethysmogramm-Analyse
für die Auswertung autonomer Arousals
Therapie
Diagnose
Diagnoseprodukt
Embla S4500
Der Embla S4500 PSG-Verstärker erfüllt die Akkreditierungsvoraussetzungen der AASM. Die Ausstattung des
Geräts wurde optimiert und besitzt ein farbcodiertes Anschlussfeld auf einem Patienten-Layout. Dieses gestraffte Zweikomponentensystem kommt mit weniger Kabeln aus und erhöht die Zuverlässigkeit der Schlafuntersuchung.
Kanäle
•
•
•
•
•
•
8 x EEG
2 x EOG
3 x EMG
1 x EKG
2 x frei definierbar
1 x Thermistor
•
•
•
•
•
•
1 x Schnarchen
1 x Körperlage
2 x Atemanstrengung
1 x Druckmesswandler
1 x Oximeter
8 x DC-Kanäle
Abgeleitete Signale
Zuverlässig und robust
Flow (Nasenkanüle)
Schnarchen (Nasenkanüle)
Atemflusslimitation/Flattening
(Nasenkanüle)
R-R Intervalle (EKG)
Sp02-Mittelwert
Sp02-Beat-to-Beat
Pulsfrequenz
Pulswelle (Plethysmogramm)
Herzfrequenz (EKG)
XFlow*
XSum*
Atemzugvolumen*
Phasenanalyse*
Atemfrequenz*
*XactTrace-Gurte
RMI*
•
•
•
Intuitives Design
•
•
•
•
•
•
•
•
•
Farbcodiertes Anschlussfeld mit Patienten-Layout
Impedanzprüfung am Patientenbett mit LED-Statusanzeige
Embla PSG-Software – leistungsstark, flexibel und
AASM-konform:
Vorteile der Embla-Sensoren
Komplette Palette an Sensoren und
Zubehör
Konkurrenzlose Genauigkeit der Messung der Atemanstrengung mittels
XactTrace-Sensoren
Zusätzliches Atemflusssignal von
XFlowTM als zuverlässiger Ausfallschutz bei Untersuchungen ohne
Atemflusssensoren
Hervorragende Nasaldruckmessung
für Atemfluss- und Schnarchsignale
Aufzeichnung von bis zu 32 Kanälen
Verfügbarkeit von zusätzlichen abgeleiteten Signalen über
die Software
Integrierter Druckmesswandler mit Luer Lock-Anschluss
aus Stahl
•
•
Zeitsparende Auswerte- und Bearbeitungsfunktionen
Optimiertes Konzept für Routineaufgaben und natürliche
Arbeitsabläufe
Beliebige Referenzierung der Kanäle während und nach
der Erfassung möglich
Einstellbare Abtastraten
Verarbeitung von zusätzlichen, mit XactTrace-Sensoren
abgeleiteten Signalen, wie Flow, Lungenvolumen und
RMI; die XactTrace-Sensoren verwenden die von der
AASM empfohlene RIP-Technologie (respiratorische Induktionsplethysmographie)
17
Therapie
Diagnose
Diagnoseprodukt
Embla N7000
Das Embla N7000-System bietet hohe Flexibilität und beste Signalqualität und entspricht so den hohen Anforderungen im klinischen Bereich und der Forschung. Der Embla N7000-Verstärker ist für eine ganze Reihe
von Aufgaben unverzichtbar, die ein Höchstmaß an Flexibilität und Effizienz in der Datenabfrage verlangen.
Das N7000-System verkörpert eine gelungene Integration von digitaler Technologie und Feinwerktechnik. Das
Resultat ist ein ergonomisches PSG und EEG-System.
Embla N7000 Spezifikationen
•
•
•
•
Insgesamt bis zu 60 Aufzeichnungen, wie z. B.:
- 32 referenzierte Kanäle (EEG, EOG)
- 8 bipolare Kanäle (EEG, EMG)
- 11 respiratorische Eingänge
- 1 Ereignis-Kanal
- 8 DC-Kanäle
Integrierter Impedanzcheck
Große Auswahl an wählbaren Abtastraten
Integrierter Umgebungslichtdetektor
Neueste Technologie für höchste Ansprüche
Abgeleitete Signale
Flow (Nasenkanüle)
Schnarchen (Nasenkanüle)
Atemflusslimitation/Abflachung (Nasenkanüle)
Herzfrequenz (EKG)
R-R Intervalle (EKG)
XFlow*
XSum*
Atemzugvolumen*
Phasenanalyse*
Atemfrequenz*
RMI* *XactTrace-Gurte
Der Embla Sensor-Vorteil
•
•
•
•
•
18
•
Sowohl für routine- und wissenschaftliche Schlafaufzeichnungen, als auch für ein komplettes 32-KanalEEG
Leistungsstarke und flexible Software
•
•
•
•
•
•
Rembrandt und Somnologica Schlafdiagnosesoftware, die auf dem Markt führend sind
Zeitsparende Auswerte- und Bearbeitungsfunktionen
Optimiert für Routineaufgabenstellungen und
natürliche Arbeitsabläufe
Option, Kanäle während und nach der Erfassung
nochmals zu re-referenzieren
Einstellbare Abtastrate
Berechnung von zusätzlichen Signalen, wie Atemfluss, Lungenvolumen und RMI, von den XactTraceGurten
Komplette Palette an Sensoren und Zubehör
Unerreichte Genauigkeit der Atemanstrengungsmessung mit Respiratorischer Induktionsplethysmographie durch XactTrace-Sensoren
Zusätzliches Atemflusssignal mit XFlow für Schlafstudien ohne Atemflusssensor oder als
verlässliche Absicherung
Hervorragende Nasaldruckmessung für Atemfluss- und Schnarchsignale
Optimierte Länge der Sensorenkabel
Therapie
Diagnose
TNI® Wirkungsweise
Allgemeine Informationen
Atemhilfe ist u.a. notwendig bei nächtlichen Atmungsstörungen (Schlafapnoen), verschiedenen Arten der respiratorischen Insuffizienz (wie z.B. die chronisch obstruktive Lungenerkrankung, COPD) und bei diversen weiteren
Indikationen in der Klinik. Ein hoher Anteil der Bevölkerung leidet unter Atemschwierigkeiten.
An Schlafapnoe leidet mindestens 4% der Bevölkerung. Zu den langfristigen
Risiken gehören Schlaganfall und Herzinfarkt. Kurzfristig führt die allnächtliche Absenkung des Sauerstoffs im Blut zu: Bluthochdruck, massiver Tagesmüdigkeit und Einschlafattacken, verantwortlich auch für Sekundenschlaf
am Steuer.
Eine Therapie ist notwendig, wird aber häufig nicht ausreichend vom Patienten angewendet, weil die entsprechende Diagnose oder die Akzeptanz der
bestehenden Therapieformen fehlt. So z.B. bei der CPAP (continuous positive airway pressure) Therapie, die nur eine Akzeptanzrate von 60-70% 1,2,3
durch bestehende Probleme mit der Beatmungsmaske hat.
Eine weltweit neue Technik zur Atemhilfe ist die Therapie mit nasaler Insufflation (TNI®)4,5,6. TNI® unterstützt die Atmung des Patienten mit einem hohen
Fluss befeuchteter und erwärmter Luft oder Luft/Sauerstoff-Mischungen. Bisher wird vorwiegend eine Überdruckbeatmung angewendet, die auf eine fest anliegende und dicht abschließende Nasen- oder Gesichtsmaske angewiesen ist.
Durch den Verzicht auf die Maske bei der TNI®-Methode treten keine der massiven Nebenwirkungen wie z.B.
Druckstellen, chronische Augenentzündungen und Angstzustände wegen des Überdrucks auf.
Dadurch ist diese einfache und anwenderfreundliche Therapieform der Atemhilfe für die Nutzung im Schlaf und
für chronisch Kranke eine echte Alternative. Die soziale und klinische Situation der Patienten wird verbessert. Die
bisher angefallenen Kosten einer Diagnosestellung und Therapieeinweisung bei Schlafapnoeikern sinken, da ein
Aufenthalt im Schlaflabor bei einem Teil der Patienten ganz entfällt.
TNI® Wirkungsweise
Messungen von der Johns Hopkins Klinik7,8 zeigten bereits,
dass die Atmung unter High-Flow-Beatmung, wie beispielsweise mit dem Gerät TNI®20, effektiv entlastet wird. Der
PEEP (positive end-expiratory pressure) wird messbar höher,
so dass der maximale inspiratorische Fluss und das Tidalvolumen erhöht werden. Dieser unterstützende Effekt erhöht
die Ventilation und verringert die Atmungsanstrengung. Als
Folge konnte auch eine Reduzierung der Atemfrequenz beobachtet werden. Dadurch eröffnet sich für die vergleichsweise angenehme atmungsunterstützende Methode im Klinikbereich neben der schlafmedizinischen Anwendung ein
großes Potential.
TNI Off
TNI 20L/min
Expiration
Flow
(ml/s)
Inspiration
PSG
Hypopnea
Hypopnea
0
(cmH2O)
-15
Microphone
100
97
95
SaO2
(%)
93
90
30s
Figure 2: Effect on Sleep Disordered Breathing
1 Rauscher H et al (1993), “Self-reported vs. measured compliance with nasal CPAP for obstructive sleep ap-nea.” Chest 103:1675-1680
2 Kribbs, NB et al (1993), “Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea.” Am. Rev. Respir. Dis.
147:887-895
3 Lavie P (1999), “Treatment of Sleep Apnea: Unmet Needs.“ Chest 116:1501-1503
4 Stoohs RA, Schneider H (2005), „Eine neue therapeutische Strategie zur Behandlung der oberen Atemwegs-obstruktion im Schlaf: Insufflation von Luft
durch eine Nasenkanüle.“ Pneumologie 2005:59
5 McGinley BM et al (2007), “A nasal cannula can be used to treat obstructive sleep apnea.” Am. J. Respir. Crit. Care Med. 176(2):194-200
6 Nilius G et al (2007), “Multicenterstudie zur Wirksamkeit der transnasalen Insufflation (TNI®) bei leichter bis mittelgradiger pharyngealer Obstruktion
und Schlafapnoe“ Somnologie 11, Supplement 1:26 [conference abstract]
7 Stoohs RA, Schneider H (2005), Eine neue therapeutische Strategie zur Behandlung der oberen Atemwegsobstruktion im Schlaf: Insufflation von Luft
durch eine Nasenkanüle [Abstrakt]. Pneumologie 59(4)
8 McGinley BM et al (2007), A nasal cannula can be used to treat obstructive sleep apnea. Am. J. Respir. Crit. Care Med. 176(2):194-200
19
Therapie
Diagnose
TNI® Wirkungsweise
Wirkungsweise 1: Erhöhung des Außendrucks
Erhöhter Widerstand nach Außen und
Verwirbelungen erhöhen den Druck
Auch ein hoher Fluss bei offener
Nase außen führt zu geringerer
Druckdifferenz
Die TNI® Therapie vermindert die Druckdifferenz, die der Atemantrieb zwischen Thorax und oberen Atemwegen erzeugt, bei
20 Liter pro Minute Fluss je nach Anatomie der oberen Atemwege um ca. 2-4 mBar.
Die Beziehung zwischen Druck und Fluss ist dabei nicht linear!
Wirkungsweise 2: Erhöhung des "PEEP"
PEEP: “Positive End Expiratory Pressure”
1. Erhöhung des PEEP
↓
2. Verbesserter inspiratorischer Fluss
↓
3. Erhöhung des Tidalvolumens
↓
•
Die TNI® Therapie
erzeugt einen PEEP
von ca. 2 – 4 mBar
•
Ersatz der
„Lippenbremse“
in der Nacht –
aktive Ausatmung
4. Verminderung der Atemarbeit
↓
5. Verschiebung des Pcrit
•
Entlastet die
Atemmuskulatur
Atemfluss
Oesophagusdruck
PEEP ohne TNI
PEEP mit TNI
Nach Schneider und Schwartz, APSS 2005
Mögliche Wirkungsweise 3: "Spannung" der oberen Atemwege?
1. Erhöhung des PEEP
2. Verminderung der Druckschwankungen während der Atmung
3. Anatomische „Streckung“ der oberen Atemwege vermindern die Kollapsibilität
Wird in wissenschaftlichen Studien untersucht
20
Therapie
Diagnose
TNI® Wirkungsweise
Mögliche Wirkungsweise 4: Erhöhung des Außendrucks
Atemfluss
Aktivierung eines Kontrollmechanismus über Rezeptoren in der Nase und/oder den oberen Atemwegen.
Hinweis: Ein Teil des Effektes ist erst nach einigen
Atemzügen zu sehen.
Oesophagusdruck
TNI ON
Wesentliche Stabilisierung
erst nach 6-7 Atemzügen
Resultate aus Studien und Tests
Erwachsene OSA
50
Events/hr
40
RDI
30
60
60
60
60
50
50
50
50
40
40
40
40
30
30
30
30
20
20
20
20
10
10
10
10
0
0
0
20
10
0
0
1
Kinder OSA
60
Total
60
NREM
40
p <0.01
40
AHI (Events/hr)
AHI (Events/hr)
30
30
20
20
20
10
10
10
0
0
BSL TNI
REM
p <0.01
40
30
Figure 3: Sleep Disordered Breathing Indices On and Off TNI
50
p <0.01
AHI (Events/hr)
60
50
50
2
Pre - Post treatment
0
BSL
TNI
BSL
TNI
21
Therapie
TNI® Wirkungsweise
Diagnose
Allgemeine Informationen zu COPD und respiratorische Insuffizienz
COPD wird nach Schätzungen bereits im Jahre 2010 die vierthäufigste Todesursache in Europa darstellen, 2002
starben weltweit 2,75 Mio. Menschen an den Folgen der Erkrankung. COPD kann nicht geheilt werden, daher ist
im Krankheitsverlauf u.a. die langfristige, häusliche Atmungsunterstützung maßgeblich. Damit die notwendige
Unterstützung der Atmung vom Patienten angenommen wird, ist eine angenehme Therapieform sehr wichtig.
Mannino et al. (2007), Global burden of COPD: risk
factors, prevalence, and future trends. The Lancet
370:765-773.
Die übliche reine Sauerstofftherapie reicht bei „Overlap Syndromen“
(z.B. Obstruktionen und COPD) nicht aus (s. Arbeitshilfe schlafbezogene Atmungsstörungen, Sozialmedizinische Expertengruppe Versorgungsstrukturen der MDK Gemeinschaft, September 2006). Hyperkapnische Patienten, also mit einem erhöhten Kohlendioxidgehalt
im Blut ( > ca. 45 mmHg) können mit CPAP in Verbindung mit O2
nicht behandelt werden, da die Rückatmung in das Gerät die CO2
Problematik verschlimmert. Das führt zum Einsatz teurer Beatmungsgeräte (BiLevel). TNI® eignet sich sehr gut für Patienten mit Overlap
Syndromen. Erste Studien zeigen, dass TNI® besser CO2 auswäscht als
CPAP und besser für die Apnoen geeignet ist als Sauerstofftherapie,
welche diese sogar verschlimmert1. Um mit der traditionellen NIV die
PaCO2 –Werte zu verbessern,werden sehr hohe Drücke benötigt (im
Durchschnitt Einatmungsdruck 27,7 +/- 5,9 cm H2O2.
Studien konnten zeigen, dass sowohl der Sauerstoffanteil in der Inspirationsluft (FIO2) als auch die Sauerstoffsättigung, gekoppelt mit einer Reduzierung der Atemfrequenz, bei einer High-Flow-Beatmungstherapie höher waren
als mit der Maske bei NIV3,4.
TNI® Wirkungsweise
Die aktuellen Ergebnisse zeigen, dass TNI ® 20 oxy die Blutgaswerte deutlich verbessert, und im Unterschied zur einfachen
Sauerstofftherapie mit niedrigen Flüssen nicht nur einen Anstieg
der Sauerstoffsättigung bewirkt, sondern auch einen Rückgang
des CO 2 Partialdrucks. Die Atmung wird nachweislich unterstützt, die Atemarbeit verringert und der Patient erholt
sich spürbar.
1 Brown C et al (2007), Treatment of Sleep-Disordered Breathing in Chronic Obstructive Pulmonary Disease with Nocturnal Nasal Insufflation. Proc. Am.
Thor. Soc. 2007: A709 [conference abstract]
2 Windisch W et al (2006), Outcome of patients with stable COPD receiving controlled noninvasive positive pressure ventilation aimed at a maximal
reduction of Pa(CO2).
3 Walsh J (2002): “Winning by a nose”. Advance for Respiratory Practioners 22.
4 Tiep B. & Barnett M. (2002): “High flow nasal vs. high flow mask oxygen delivery: tracheal gas concentrations through a head extension airway model”, Respir. Care 47(9).
22
Therapie
Diagnose
TNI® Wirkungsweise
BGA Gruppen unter herkömmlicher Therapie
Progression der
Respiratorischen Insuffizienz
Gruppe 1: paO2 ↑ und paCO2 ↓
► wünschenswert
Gruppe 2: paO2 ↑ und paCO2 =
► akzeptabel
Gruppe 3: paO2 ↑ und paCO2 ↑
► Problem
Gruppe 4: paO2 = und paCO2 =↑ ► großes Problem
NIV
Nächtliche Hypoventilation
Vorbote der nächsten Stufe
•Lippenbremse
Resp. Insuffizienz
LTOT
Kaum merklich
TNI
CO2 - Auswaschung durch TNI®
TNI+O2
Applikator
Zeit
TNI anstatt NIV
Luft-/Sauerstoff Gemisch
CO2
Fallbeispiele respiratorischer Insuffizienz
23
Therapie
Diagnose
TNI® Wirkungsweise
TNI® Wirkungsweise bei COPD
TNI® ...
• verwirbelt das Luft-O2-Gemisch im Totraumvolumen.
• erhöht dadurch die Ventilation und sorgt für eine CO2-Auswaschung.
• verbessert die Atemeffizienz: (VD/VT) und damit die Belüftung der Lunge
(VA).
• reichert das VD mit „brauchbarem“ Luft-O2-Gemisch an.
• vermindert den arteriellen CO2 Gehalt durch die Verbesserung der VA.
(Mit Verabreichung von nur reinem Sauertoff nicht erreichbar.)
• wärmt und befeuchtet den beigemischten Sauerstoff.
• verbessert das Abhusten durch die feuchte und warme Luft.
• ist nebenwirkungsfrei.
• die positiven Ergebnisse können in der BGA nachgewiesen werden.
...
24
IST EINE NEUE
THERAPIE
Therapie
TNI® Studien
Diagnose
25
Therapie
TNI® Studien
26
Diagnose
Therapie
TNI® Studien
Diagnose
27
Therapie
TNI® Studien
28
Diagnose
TNI® Studien
Therapie
Diagnose
Correct Citation for publication:
Treatment of Sleep-Disordered Breathing in Chronic Obstructive Pulmonary Disease with Nocturnal
Nasal Insufflation. C.D. Brown, M.D., L.B. Herpel, M.D., K.L. Goring, M.D., P.L. Smith, M.D., R.A. Wise,
M.D., H. Schneider, M.D., Ph, A.R. Schwartz. Proc Am Thor Soc 2007,, A709
Poster Board #F64] Treatment of Sleep-Disordered Breathing in Chronic Obstructive Pulmonary
Disease with Nocturnal Nasal Insufflation, [Publication Page: A709]
C.D. Brown, M.D., L.B. Herpel, M.D., K.L. Goring, M.D., P.L. Smith, M.D., R.A. Wise, M.D., H. Schneider,
M.D., Ph, A.R. Schwartz, M.D., Baltimore, MD
Introduction: Sleep-disordered breathing (SDB) with inspiratory flow limitation (IFL) is common in patients
with COPD, even without frank apneas or hypopneas. Nocturnal nasal insufflation (NNI) may relieve IFL and
upper airway obstruction during sleep to improve gas exchange and sleep quality in COPD.
Methods: Non-hypoxemic individuals with a wide range of COPD severity underwent baseline
polysomnography to determine the severity of sleep-disordered breathing. On a separate night, subjects
were exposed to alternating trials of NNI (20 L/min), oxygen (2 L/min), and room air during NREM sleep.
SDB indices including arousal-terminated IFL event rates, the apnea-hypopnea index (AHI) and
transcutaneous carbon dioxide (TcCO2) were compared among conditions.
Results: NNI decreased the arousal frequency, AHI, and TcCO2 from the room air and oxygen conditions.
NNI resulted in a 50% reduction in IFL events compared to room air (p=0.04) whereas oxygen was
associated with a 120% increase in IFL events. TcCO2 increased during oxygen treatment and fell during
NNI compared to the room air condition (Figure 1, p=0.001 for NNI vs. room air).
Conclusion: NNI decreased SDB and improved nocturnal ventilation in patients with COPD. The CO2
response to NNI suggests that IFL contributes to the development of nocturnal hypoventilation in COPD and
that NNI may constitute a novel treatment for SDB in COPD.
29
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Diagnose
Predictors for Treating Obstructive Sleep
Apnea With an Open Nasal Cannula System
(Transnasal Insufflation)
Georg Nilius, Thomas Wessendorf, Joachim Maurer, Riccardo Stoohs,
Susheel P. Patil, Norman Schubert and Hartmut Schneider
Chest 2010;137;521-528; Prepublished online December 1, 2009;
DOI 10.1378/chest.09-0357
The online version of this article, along with updated information
and services can be found online on the World Wide Web at:
http://chestjournal.chestpubs.org/content/137/3/521.full.html
CHEST is the official journal of the American College of Chest
Physicians. It has been published monthly since 1935. Copyright 2010
by the American College of Chest Physicians, 3300 Dundee Road,
Northbrook, IL 60062. All rights reserved. No part of this article or PDF
may be reproduced or distributed without the prior written permission
of the copyright holder.
(http://chestjournal.chestpubs.org/site/misc/reprints.xhtml)
ISSN:0012-3692
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CHEST
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Original Research
SLEEP MEDICINE
Predictors for Treating Obstructive Sleep
Apnea With an Open Nasal Cannula System
(Transnasal Insufflation)
Georg Nilius, MD; Thomas Wessendorf, MD; Joachim Maurer, MD; Riccardo Stoohs, MD;
Susheel P. Patil, MD, PhD; Norman Schubert, R-PSGT; and Hartmut Schneider, MD, PhD
Background: Obstructive sleep apnea (OSA) is a disorder that is associated with increased morbidity and mortality. Although continuous positive airway pressure effectively treats OSA, compliance is variable because of the encumbrance of wearing a sealed nasal mask throughout sleep. In
a small group of patients, it was recently shown that an open nasal cannula (transnasal insufflation
[TNI]) can treat OSA. The aim of this larger study was to find predictors for treatment responses
with TNI.
Methods: Standard sleep studies with and without TNI were performed in 56 patients with a wide
spectrum of disease severity. A therapeutic response was defined as a reduction of the respiratory
disturbance index (RDI) below 10 events/h associated with a 50% reduction of the event rate
from baseline and was used to identify subgroups of patients particularly responsive or resistant
to TNI treatment.
Results: For the entire group (N 5 56), TNI decreased the RDI from 22.6 6 15.6 to 17.2 6 13.2
events/h (P , .01). A therapeutic reduction in the RDI was observed in 27% of patients. Treatment
responses were similar in patients with a low and a high RDI, but were greater in patients who
predominantly had obstructive hypopneas or respiratory effort-related arousals and in patients
who predominantly had rapid eye movement (REM) events. The presence of a high percentage
of obstructive and central apneas appears to preclude efficacious treatment responses.
Conclusion: TNI can be used to treat a subgroup of patients across a spectrum from mild-to-severe
sleep apnea, particularly if their sleep-disordered breathing events predominantly consist of
obstructive hypopneas or REM-related events but not obstructive and central apneas.
CHEST 2010; 137(3):521–528
Abbreviations: CPAP 5 continuous positive airway pressure; NREM 5 nonrapid eye movement; OSA 5 obstructive
sleep apnea; RDI 5 respiratory disturbance index; REM 5 rapid eye movement; RERA 5 respiratory effort-related
arousal; TNI 5 transnasal insufflation; TST 5 total sleep time
sleep apnea (OSA) is a common disorObstructive
der that is associated with increased morbidity
and mortality.1,2 Continuous positive airway pressure
(CPAP) is the only treatment shown to reduce both
cardiovascular and neurobehavioral morbidities.3,4
Approximately 25% to 50% of patients with OSA will
either refuse or not tolerate the use of CPAP
therapy,5,6 primarily because of the mask and head
gear required for maintaining positive pressure during sleep.7,8 Thus, improvements in nasal interfaces
and overall comfort might improve adherence to
therapy.
Manuscript received February 10, 2009; revision accepted
September 24, 2009.
Affiliations: From the HELIOS-Klinik Hagen-Ambrock Germany (Dr Nilius), University Witten-Herdecke; Ruhrlandklinik
(Dr Wessendorf), Essen, Germany; HNO-Klinik der Universität
(Dr Maurer), Mannheim, Germany; Somnolab (Dr Stoohs), Dortmund, Germany; and the Department of Pulmonary and Critical
Care Medicine (Drs Patil and Schneider, Mr Schubert), Johns
Hopkins University, Baltimore, MD.
Funding/Support: This study was sponsored by Selion Inc.
(HL 72126, P50 HL084945-01).
Correspondence to: Georg Nilius, MD, Ambrocker Weg 60,
58091 Hagen, Germany; e-mail: [email protected]
© 2010 American College of Chest Physicians. Reproduction
of this article is prohibited without written permission from the
American College of Chest Physicians (www.chestpubs.org/
site/misc/reprints.xhtml).
DOI: 10.1378/chest.09-0357
www.chestpubs.org
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Recently, it has been demonstrated that the transnasal insufflation (TNI) of warm and humidified air
at a flow rate of 20 L/min through an open nasal cannula system led to a therapeutic reduction of the
sleep-disordered event rate in approximately onethird of the patients studied.9 Because of the small
number of patients studied, it was not possible to
determine polysomnographic predictors for treatment
responses.
In the current study, we examined the polysomnographic responses to TNI in a larger clinical sample
of patients. The primary goal of this study was to
identify polysomnographic characteristics on a baseline sleep study that may be used to predict TNI
treatment responses. Because the major mechanism
of action of TNI appears to be through a small
increase in end-expiratory pharyngeal pressure, lower
levels of pressure should be sufficient to alleviate
hypopneas.4,10 We therefore hypothesized that TNI
would have a positive therapeutic effect in patients
with sleep-disordered breathing and that TNI would
be more effective in treating patients who predominantly have hypopneas rather than apneas.
Materials and Methods
The study was conducted under the supervision of the ethics
committees of the Universität Witten-Herdecke and according to
“Good Clinical Practices” and the Declaration of Helsinki.11 In
addition, the study was reviewed and approved by the institutional
review board of each participating center, including the reading
center at the Johns Hopkins Sleep Disorders Center, which
scored all sleep studies and performed the data analysis. Study
procedures, risks, and benefits were reviewed, and written informed
consent was obtained for each participant prior to enrollment in
the study.
Subjects
Recruitment of participants for the study was conducted
at four sleep disorder centers between November 2006 and
August 2007. Participants were eligible if they met all of the following inclusion criteria: (1) a baseline sleep study that demonstrated a total nonrapid eye movement (NREM) and rapid eye
movement (REM) sleep stage respiratory disturbance index
(RDI) of . 5 events per hour, (2) presence of excessive daytime
sleepiness by self-report, (3) clinical criteria for CPAP treatment
according to the standard practice of care of each sleep laboratory, (4) patients had not previously used CPAP in the management of their disease, and (5) a CPAP titration study that
demonstrated a nasal pressure less than the median prescribed
pressure of each laboratory (range of CPAP pressure was from
8-11 cm H2O).
Patients were excluded from participating in the study, if they
had significant comorbidities, including (1) a past surgery of the
nose or pharyngeal structure in the last 12 months or other medical and mechanical treatment of OSA; (2) other sleep-associated
disorders, such as restless leg syndrome, periodic leg movement
disorder, central sleep apnea disorders, or Cheyne-Stokes breathing; (3) lung disorders (COPD) and heart failure; and (4) bleeding
disorders or use of oral anticoagulation medication.
522
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Study Materials
Polysomnography: Standard sleep studies were conducted
using the study sites’ local recording platform (Alice [Respironics
Deutschland GmbH & Co. KG; Herrsching, Germany], Rembrandt [Medcare Deutschland GmbH; Wessling, Germany],
Somnologica [Embla Systems GmbH; Munich, Germany], and
Jaeger [VIAASYS Healthcare GmbH; Höchberg, Germany]) according to standard clinical practice of each center and the guidelines
of the German Sleep Medicine Society (Deutsche Gesellschaft
fuer Schlafmedizin). All sleep studies consisted of the following
signals: EEG (montage C3/A2 and C4/A4); right and left electrooculogram; chin, left and right leg electromyogram; a single, bipolar
ECG; oxyhemoglobin saturation by finger pulse oximeter; nasal and
oral airflow monitored by a nasal pressure transducer and an oronasal
thermistor; chest and abdominal excursions by inductive plethysmography or strain gauges; snoring sounds with a neck microphone; and
body position by a mercury gauge and video monitoring.
Recordings were stored in real time (European Data Format) and
sent to a central reading center at the Johns Hopkins Sleep Disorders
Center via an independent study monitoring agency (Marshall
Assoc.; Maxismedical; Frankfurt, Germany). At the reading center,
recordings were first deidentified and formatted to provide uniform
scoring platforms for all studies. Sleep studies were scored by experienced registered polysomnographic technicians who were unaware
of the purpose and hypotheses of the current study. Finally, all scored
sleep studies were reviewed by a Diplomate of American Board of
Internal Medicine, Sleep Medicine (S. P. P.), who was also masked to
the treatment status. Polysomnographic indices were then entered
into a custom-made database after quality assurance assessments
confirmed reliability for scoring and reviewing sleep stages, respiratory events, and respiratory arousals, as previously published.9
Study Protocols
The study protocol consisted of three consecutive nights. Night
1 (baseline sleep study) was used for characterizing standard sleep
and breathing indices off TNI. Night 2 (CPAP titration study) was
used for the stepwise increase in nasal pressure and the observation
of the airflow signal from the built-in pneumotachographs of the
CPAP devices. The effective nasal pressure for CPAP was defined as
the pressure at which inspiratory flow limitation was abolished and a
normal non-flow limited airflow contour ensued during NREM and
REM sleep. On the third night (TNI treatment night), participants
were asked to initiate sleep on 10 L/min on TNI for reasons of comfort. After lights out, TNI was then increased in a ramplike fashion
(automatically) to 20 L/min over a period of 5 to 10 min.
Sleep Study Analysis
Polysomnographic indices were obtained from sleep studies
that had at least 240 min of recording time or 180 min of sleep,
and signal quality of airflow and respiratory effort belts allowed
discerning the type and duration of sleep-disordered respiratory
events. Out of a total of 65 enrolled patients, 56 patients met these
criteria. Sleep stages and arousal were defined according to published criteria.12 Respiratory events were defined as follows:
Obstructive apnea and presence of central sleep apnea was identified
if the airflow was absent or nearly absent for at least 10 s. Hypopnea was identified when there was a . 30% reduction in airflow
that was associated with a decrease in oxyhemoglobin desaturation
of more than 3%. In addition, respiratory effort-related arousals
(RERAs) were identified as a series (more than three breaths) of
flow-limited breaths that demonstrated either a discernible reduction in airflow from baseline of , 30% or an increase in respiratory
effort without concordant increases in airflow that was terminated
by an arousal. Central apnea was identified if the absence of airflow was associated without discernable excursions of either the
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chest or abdomen. The RDI was defined as the number of apneas,
hypopneas, and RERAs per hour for NREM, REM, and total
sleep. The predominance of specific events was used to define
three subgroups with mild upper airway obstruction: (1) Patients
with increasing proportions of obstructive hypopneas were identified by the percent rate of hypopneas, which was computed by
calculating the proportions of obstructive hypopneas to all respiratory events (apneas, hypopneas, and RERAs) for each patient
during NREM sleep and creating subgroups of patients with
increasing proportions of hypopneas (. 50%, . 66%, and . 90%
hypopneas, respectively). (2) Patients with a predominance of
RERAs (upper airway resistance syndrome) were identified if
the apnea and hypopnea rate was , 10 events/h and if they had an
RERAs to apnea + hypopnea ratio of . 2:1. (3) Patients with
REM-dependent sleep-disordered breathing had a NREM event
rate of , 10 events/h and a REM-to-NREM event ratio of . 2:1,
as described previously.13,14
Statistical Analysis
The primary outcome of treatment efficacy of TNI was defined
as follows: for individuals with a baseline RDI . 10 events/h, if
the RDI fell more than 50% and below 10 events/h sleep, and for
individuals whose baseline RDI was , 10, if the RDI fell below
five events/h and by more than 50% from baseline. Based on the
findings of the previous study,9 a sample size calculation revealed
that 40 subjects were needed with 80% power and type 1 error of
5% in order to detect a change in RDI of 20 events/h. A paired
Student t test was used to compare the RDI between baseline and
treatment conditions in all sleep states.
In secondary analyses, we examined potential polysomnographic, demographic, and anthropometric factors that might predict a treatment response or nonresponse to TNI. These factors
included the effects of age, sex, BMI, prescribed CPAP pressure,
the proportion of hypopneic events, and central sleep apnea.
To determine whether the treatment responses observed differed from normal night-to-night variability of the RDI, we first
determined the proportion of patients that were effectively treated
for the entire group and for subgroups with increasing proportions of hypopneas (. 50%, . 66%, and . 90% hypopneas,
respectively). Since the treatment night was not randomized, the
observed therapeutic effects of TNI may be attributed to the
expected spontaneous night-to-night variability in sleep apnea
severity. We therefore compared TNI response rates to the reported
night-to-night variability in sleep apnea severity reported in the
study of Stepnowsky et al,15 (13%), using the one-sample test of
proportions. In the subset of patients who predominantly have
REM-related obstructive sleep apnea, the Wilcoxon matchedpairs signed-rank test was used to compare differences between
baseline and treatment condition, because of the nonnormal distribution of the data.
Diagnose
Table 1—Anthropometric and Polysomnographic
Indices at Baseline
Data
Numbers
Sex, male (female)
42 (12)
Age, y
50.5 6 10.4
2
BMI, kg/m
28.0 6 3.5
Polysomnographic indices
Prescribed CPAP, cm H2O
7.5 6 1.9
TST, min
332.0 6 65.0
SE, % TST
82.2 6 12.2
N1, % TST
14.0 6 11.8
N2, % TST
56.3 6 12.7
N3, % TST
10.7 6 9.5
REM, % TST
19.0 6 7.0
RDI, events/h
22.6 6 15.6
NREM-RDI, events/h
21.9 6 16.4
REM-RDI, events/h
24.4 6 21.3
Sleep apnea subgroups
Predominance of RERAs (UARS), No. of patients (%)
3 (5)
REM event predominance, No. of patients (%)
11 (20)
26 (46)
Predominance of hypopneas (. 50%), No. of
patients (%)
16 (29)
Predominance of apneas (. 50%), No. of patients (%)
CPAP 5 continuous positive airway pressure; N1 5 sleep stage 1; N2 5
sleep stage 2; N3 5 sleep stage 3; NREM 5 nonrapid eye movement;
RDI 5 respiratory disturbance index; REM 5 rapid eye movement;
RERA 5 respiratory effort-related arousal; SE 5 sleep efficiency; TST 5
total sleep time; UARS 5 upper airway resistance syndrome.
Polysomnographic Responses to TNI
Figure 1 shows mean and individual responses
of the RDI to TNI compared with baseline for
the entire night, and for NREM and REM sleep stages.
On average, TNI led to a slight reduction of the RDI
in NREM, REM, and the entire night, due to heterogeneous response rates between participants.
Although TNI decreased RDI in the majority of
patients, eight participants demonstrated a marked
increase in the RDI (as defined by in increase of more
Results
Subjects
Table 1 shows the anthropometric and polysomnographic characteristics of the baseline sleep study of all
participants. The study population consisted mostly of
men (79%). The majority of patients had obstructive
hypopnea or obstructive apnea, suggesting a moderateto-severe degree of upper airway obstruction, whereas
only a minority had milder degrees of upper airway
obstruction (upper airway resistance syndrome, n 5 3;
or predominant REM events, n 5 11).
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Figure 1. Responses of RDI to TNI. 5 mean ± SD; x 5 example of a single responder (see Figure 2, case 1); * 5 example of
a nonresponder (see Figure 2, case 2); NREM 5 nonrapid eye
movement; RDI 5 respiratory disturbance index; REM 5 rapid
eye movement; TNI 5 transnasal insufflation.
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than 10 events/h compared with baseline) due to
positional apneas and technical limitations. (See Limitations in “Discussion” section.)
Figure 2 shows the respiratory pattern at baseline
and on TNI in one patient (see asterisk in Fig 1) who
had a complete resolution of sleep-disordered breathing (Fig 2A) and in another patient (see x in Fig 1)
in whom the RDI increased significantly with TNI
(Fig 2B). In the patient shown in Figure 1A, TNI
abolished inspiratory flow limitation and stabilized
the breathing pattern. In contrast, in the patient shown
in Figure 1B the RDI increased from 20 to 58 events/h
because of a positional effect on sleep apnea severity.
This patient spent considerably more time supine on
the treatment night compared with baseline (43% vs
23% total sleep time [TST], respectively). When
comparing the RDI for the supine position, the RDI
decreased from 72 events/h with 54% apneas to
51 events/h with no apneas. Thus, albeit there was no
clinical efficacious reduction in the RDI, TNI converted apneas to hypopneas.
For the entire group, we observed that TNI led to
a conversion of apneas to hypopneas without increasing the rate of RERAs. Specifically, the percent rate of
apneas to all events (apneas/hypopneas and RERAs)
decreased from 46.3% 6 4.4% to 18.4% 6 4.1%
(P , .05) during REM sleep and 34.4% 6 7.4% vs
27.4% 6 8.1% TST (not significant) during NREM
sleep. The rate of RERAs during NREM and REM
sleep combined was 5.8 6 0.9 events/h at baseline
and 3.9 6 0.5 events/h at treatment night on TNI.
Diagnose
Predictors for Efficacious Responses to TNI
Anthropometric and Clinical Characteristics; Event
Type and Rate: Anthropometric characteristics, including sex, age, BMI, prescribed CPAP pressure, and
baseline polysomnograph, indies, did not differ between
those participants who met our definition for a response
to those who had a suboptimal reduction in the RDI
(see Table 2). Figure 3 shows how polysomnographic
characteristics including sleep apnea severity (Fig 3A),
event type (Fig 3B), and the degree of upper airway
obstruction as defined by the proportion of hypopneas
to all events in percent (Fig 3C) influence the response
rate to TNI. First, we found that RDI did not predict
response rates to TNI (Fig 3A). Second, in the eight
individuals who had .10 % central apneas at baseline
(Fig 3B), none had a positive response rate to TNI. The
response rate was greatest in patients who predominantly had obstructed compared with central events.
Third, a greater hypopnea rate was associated with an
increased response rate in a dose-dependent fashion
(Fig 3C). Although patients who predominantly had
apneas (. 50% of all events) had a low response rate of
18.8% (three of 16 patients), the response rate increased
from 33% (. 50% hypopnea), 38% (. 66% hypopnea),
and to 50% (. 90% hypopnea) with increasing
degrees of hypopneas, respectively. The response rate
to TNI was significantly greater in all patients with
obstructive events (Fig 3B) and all groups independent
of the proportion of hypopneas (Fig 3C) compared with
the expected night-to-night variability in sleep apnea
severity of 13%.15
Figure 2. Respiratory pattern of a responder. (A) Case 1, marked with x in Fig 1. (B) Case 2, a
nonresponder (marked with * in Fig 1). Spo2 (%) 5 oxyhemoglobin saturation. See Figure 1 legend for
expansion of other abbreviations.
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Table 2—Comparison of Anthropometric and Clinical
Data Between Responder and Nonresponder
Variable
Sex, male (female)
Age, y
BMI, kg/m2
Prescribed CPAP,
cm H2O
TST, min
SE, % TST
N1, % TST
N2, % TST
N3, % TST
REM, % TST
RDI, events/h
NREM-RDI,
events/h
Suboptimal Response
Therapeutic Response
34 (7)
50.1 6 10.0
28.4 6 3.1
7.6 6 1.9
15 (5)
51.5 6 11.7
26.8 6 4.3
7.1 6 1.9
334.2 6 69.8
81.0 6 0.1
14.0 6 0.1
58.0 6 0.1
9.0 6 0.1
19.0 6 0.1
21.6 6 15.0
20.9 6 15.1
325.9 6 48.7
84.0 6 0.1
15.0 6 0.2
52.0 6 0.2
14.0 6 0.1
19.0 6 0.1
25.2 6 17.5
24.6 6 19.7
See Table 1 for expansion of abbreviations.
Subgroups With Mild Upper Airway Obstruction:
A predominance of RERAs (upper airway resistance
syndrome) was observed in three individuals at baseline and in six on TNI. The total RDI decreased
in two individuals below five events/h, and the third
developed central apneas on TNI at a rate of
12 events/h, offsetting the reduction in RERAs in individuals with REM-sleep-disordered breathing.
A predominance of REM-sleep-disordered breathing
was observed in 10 individuals at baseline and five
on TNI. As shown in Figure 4A, all but one individual
with REM-sleep-disordered breathing at baseline
reduced the REM RDI on TNI (mean decrease from
24.3 6 2.0 to 11.6 6 2.9 events/h). The nonresponder
slept predominantly on his side during the baseline
sleep study but mostly supine during TNI treatment
night. For this group, 55% had an efficacious decrease
in REM RDI as defined above (Fig 4B). Moreover,
four of the 10 individuals decreased the total RDI
below five events/h.
Discussion
In this study, we confirmed that TNI reduced the
overall sleep-disordered breathing event rate below a
clinically acceptable threshold in approximately onequarter of patients who required CPAP therapy. Our
findings indicate that: (1) Patients with a wide range of
RDI had similar response rates, indicating that treatment responses to TNI are independent of the sleep
apnea disease severity. (2) The response rate was
markedly increased in patients who predominantly
had hypopneas and patients with mild upper airway
obstruction as indicated by a predominance of RERAs
and REM-related events. (3) The presence of . 10%
central apneas predicted poor response. (4) Anthropometric characteristics and the level of prescribed
CPAP pressure did not predict treatment responses.
Thus, TNI treatment responses depend on the severity,
but not the frequency, of upper airway obstruction.
Predictors of Response to TNI
As in our prior TNI pilot study,9 we found that TNI
reduced apneas and hypopneas. The major reason for
decreased RDI can be attributed primarily to the
increase in pharyngeal pressure that is associated with
an increase in the inspiratory airflow.16 At a rate of
20 L/min, TNI increases nasal pressure by approximately 2 cm H2O and increases inspiratory airflow
by approximately 100 mL/s.9 In general, the peak
inspiratory airflow for hypopneas and for flow-limited
breaths averages approximately 150 to 200 mL/s.10
Figure 3. Predictors of efficacious responses to TNI. RERAS 5 respiratory effort-related arousals. See
Figure 1 legend for expansion of abbreviations.
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Diagnose
sleep.26 Our current data suggest that response rates
to TNI would also be higher in adults with a predominance of REM-sleep-disordered breathing events.
Predictors of No Response to TNI
Figure 4. TNI efficacy to REM sleep apnea. See Figure 1 legend
for expansion of abbreviations.
The additional flow from TNI, therefore, will increase
the inspiratory airflow to 250 to 300 mL/second, a
level previously associated with stabilization of breathing patterns.10,17,18 In the current study, we did not
quantify airflow; thus, it was not possible to determine whether the individuals with hypopnea who did
not respond had more severe upper airway obstruction
as reflected by reduced levels of inspiratory airflow.
Additional, nonquantifiable factors that may have
contributed to the therapeutic response include the
following: First, small increases in pharyngeal pressure
may have increased lung volume, which may improve
both oxygen stores and upper airway patency.19-21
Second, as ventilation improves during sleep, enhanced
sleep continuity (decreased arousal frequency) may
further stabilize breathing and reduce the RDI.22,23
Finally, additional benefits may have accrued from
insufflating air directly into the nose, producing concomitant reductions in dead space ventilation.
REM Sleep Apnea: TNI was more effective in
improving sleep-disordered breathing in REM sleep
compared with NREM sleep, as indicated by a shift
from apneas to hypopneas for REM events and by
the response rate in individuals with predominant
REM apneas in which all but one patient had a significant reduction in the REM event rate with TNI.
REM sleep is associated with a loss in muscular tone
and a decrease in ventilatory demand. It is possible
that small increases in pharyngeal pressure are more
effective in stabilizing upper airway musculature in
the presence of a hypotonic musculature of the pharynx and chest wall during REM sleep as compared
with a more tonic state in NREM sleep.24,25 Alternatively, TNI might have increased tidal inspiratory volumes and satisfied patient’s ventilatory demand
during REM sleep. Regardless of the mechanism,
our finding is comparable to that of a recently documented study in which a high response rate to TNI
was observed in children if they had predominant
REM events but flow limitation during NREM
526
Patients with predominate obstructive or central
apneas (. 50% apneas to all events) responded poorly
(three of 18, 16.6%) to TNI for several reasons. First,
as noted, inspiratory airflow would be expected to
increase to a maximum of 100 mL/s at a TNI flow rate
of 20 L/min.9 In patients with apnea, such an increase
in airflow would not be enough, would correspond to
hypopneas, and would not eliminate sleep-disordered
breathing altogether.27,28 Second, in patients with a
significant proportion of central sleep apnea, it is possible that the additional airflow from TNI led to an
exaggeration of ventilatory overshoot.22,29 Third, it is
possible the insufflation of air into the nose may have
washed out the anatomic dead space, which may have
reduced CO2 rebreathing and thereby contributed to
the occurrence of central apneas. Further studies are
required to explore possible mechanisms.
Limitations
There are several limitations that merit consideration. First, nine initially enrolled patients were
excluded from the analysis because the sleep studies
did not meet our criteria for study participation as
mentioned in the “Methods” section. We do not
believe that the exclusion affected our results because
insufficient sleep at baseline rather than at TNI nights
was the primary reason for exclusion. Second, our primary intention was to emulate usual clinical care,
which includes changes in body position and displacement of the nasal cannula (which occurred), and thus
the effectiveness of therapy in certain individuals was
underestimated. The major limitation of the study was
the lack of quantification of airflow that might have
helped to predict responses to TNI more accurately.
We predict that patients with RERAs or hypopneas of
at least 150 mL/s would be the most likely to respond
for the reasons noted above.
Additional logistical concerns include the following:
First, we did not determine the night-to-night variability of the RDI in our study population. Instead, we used
reported night-to-night variability in RDI. The therapeutic response rate was twice as high as the 13% one
would anticipate, making polysomnographic responses
to TNI most likely attributable to the mechanisms of
action as discussed above. Second, all patients were
first titrated on CPAP according to clinical standards in
each laboratory. Although a comparison on the efficacy
of CPAP vs TNI would be potentially of interest, it
would have required randomizing TNI and CPAP
nights, which was beyond the scope of the current
Original Research
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© 2010 American College of Chest Physicians
36
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study. Finally, we observed an increase in the RDI in
eight individuals. Increases were related to (1) positional sleep apnea (n 5 5), wherein subjects spent disproportionately more time supine with TNI compared
with the baseline, (2) an inadvertent reduction the TNI
flow rate below 17 L/min (n 5 1), and (3) an increase in
central apneas on the night with TNI (n 5 2). These
limitations have to be considered in future clinical trials.
Clinical Implication
TNI offers an alternative to the standard CPAP
therapy in patients who predominantly have obstructive hypopnea. The efficacy of TNI can be easily
assessed within a single night and can be predicted
on the basis of the presence of at least 90% hypopnea
and RERAs. It is of note that a predominance of hypopneas are seen in children,30,31 and RERAs are seen in
patients with upper airway resistance syndrome32 and
females with fibromyalgia;33 therefore, these populations may be ideal for this form of therapy. Finally,
more precise measurements of inspiratory airflow
may provide a quantitative way of predicting patients
who will respond to TNI. Thus, further trials, on subgroups of patients with sleep-disordered breathing
using TNI over a longer period of time are necessary
to determine its clinical usefulness.
Acknowledgments
Author contributions: Dr Nilius: contributed to conception and
design of the study, acquisition of data in the study center Hagen,
analysis and interpretation of data, draft of article, critical revision,
and final approval.
Dr Wessendorf: contributed to conception and design of the study,
acquisition of data in the study center Essen, critical revision of
the draft, and final approval.
Dr Maurer: contributed to conception and design of the study,
acquisition of data in the study center Mannheim, critical revision
of the draft, and final approval.
Dr Stoohs: contributed to conception and design of the study,
acquisition of data in the study center Dortmund, critical revision
of the draft, and final approval.
Dr Patil: contributed to conception and design of the study, analysis
of the data in the central reading center, statistical analysis, draft of
the article, critical revision of the draft, and final approval.
Dr Schubert: contributed to analysis of the data in the central
reading center, statistical analysis, critical revision of the draft, and
final approval.
Dr Schneider: contributed to conception and design of the study,
interpretation of data, draft of article, critical revision, and final
approval.
Financial/nonfinancial disclosures: The authors have reported
to CHEST the following conflicts of interest: Dr Nilius has
received funds from Weimann, Heinen und Löwenstein, and
Fisher & Paykel. Dr Wessendorf has received funds from ResMed.
Dr Maurer has received funds from Weinmann, Heinen &
Löwenstein, MPV Truma, and ResMed. Funding for the study on
TNI described in this presentation was in part provided by Seleon
GmbH. Under a separate licensing agreement between Seleon
GmbH and the Johns Hopkins University, Dr Schneider is entitled
to a share of royalties received by the University on sales of
products described in this manuscript. The terms of this arrangement are being managed by the Johns Hopkins University in
accordance with its conflict of interest policies. Drs Stoohs, Patil,
www.chestpubs.org
Diagnose
and Schubert have reported to CHEST that no potential conflicts
of interest exist with any companies/organizations whose products
or services may be discussed in this article.
References
1. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoeahypopnoea with or without treatment with continuous
positive airway pressure: an observational study. Lancet.
2005;365(9464):1046-1053.
2. Young T, Peppard P, Palta M, et al. Population-based study of
sleep-disordered breathing as a risk factor for hypertension.
Arch Intern Med. 1997;157(15):1746-1752.
3. Aloia MS, Ilniczky N, Di Dio P, Perlis ML, Greenblatt DW,
Giles DE. Neuropsychological changes and treatment compliance in older adults with sleep apnea. J Psychosom Res.
2003;54(1):71-76.
4. Giles TL, Lasserson TJ, Smith BH, White J, Wright J, Cates
CJ. Continuous positive airways pressure for obstructive
sleep apnoea in adults. Review. Cochrane Database Syst Rev.
2006;19(3):CD001106.
5. Dinges DF, Kribbs NB, Schwartz AR, et al. Objective measurement of nasal continuous positive airway pressure use: ethical
considerations. Am J Respir Crit Care Med. 1994;149(2):291292.
6. McArdle N, Devereux G, Heidarnejad H, Engleman HM,
Mackay TW, Douglas NJ. Long-term use of CPAP therapy
for sleep apnea/hypopnea syndrome. Am J Respir Crit Care
Med. 1999;159(4 Pt 1):1108-1114.
7. Weaver TE, Laizner AM, Evans LK, et al. An instrument to
measure functional status outcomes for disorders of excessive
sleepiness. Sleep. 1997;20(10):835-843.
8. Stepnowsky CJ Jr, Marler MR, Ancoli-Israel S. Determinants
of nasal CPAP compliance. Sleep Med. 2002;3(3):239-247.
9. McGinley BM, Patil SP, Kirkness JP, Smith PL, Schwartz AR,
Schneider H. A nasal cannula can be used to treat obstructive
sleep apnea. Am J Respir Crit Care Med. 2007;176(2):194-200.
10. Gleadhill IC, Schwartz AR, Schubert N, Wise RA, Permutt
S, Smith PL. Upper airway collapsibility in snorers and in
patients with obstructive hypopnea and apnea. Am Rev Respir
Dis. 1991;143(6):1300-1303.
11. World Medical Association Declaration of Helsinki. Ethical
principles for medical research involving human subjects.
JAMA, 2000;284:3043-3045.
12. Iber C, Ancoli-Israel S, Chesson AL, Quan SF. The AASM
Manual for the Scoring of Sleep and Associated Events: Rules,
Terminology and Technical Specifications. Westchester, IL;
American Academy of Sleep Medicine; 2007.
13. Koo BB, Dostal J, Ioachimescu O, Budur K. The effects of
gender and age on REM-related sleep-disordered breathing.
Sleep Breath. 2008;12(3):259-264.
14. Haba-Rubio J, Janssens JP, Rochat T, Sforza E. Rapid eye
movement-related disordered breathing: clinical and polysomnographic features. Chest. 2005;128(5):3350-3357.
15. Stepnowsky CJ Jr, Orr WC, Davidson TM. Nightly variability of sleep-disordered breathing measured over 3 nights.
Otolaryngol Head Neck Surg. 2004;131(6):837-843.
16. Smith PL, Wise RA, Gold AR, Schwartz AR, Permutt S.
Upper airway pressure-flow relationships in obstructive sleep
apnea. J Appl Physiol. 1988;64:789-795.
17. Patil SP, Schneider H, Marx JJ, Gladmon E, Schwartz AR,
Smith PL. Neuromechanical control of upper airway patency
during sleep. J Appl Physiol. 2007;102(2):547-556.
18. Schneider H, O’Hearn DJ, Leblanc K, et al. High-flow transtracheal insufflation treats obstructive sleep apnea. A pilot
study. Am J Respir Crit Care Med. 2000;161(6):1869-1876.
CHEST / 137 / 3 / MARCH, 2010
527
Downloaded from chestjournal.chestpubs.org at Welch Medical Library - JHU on April 13, 2010
© 2010 American College of Chest Physicians
37
Therapie
TNI® Studien
19. Heinzer RC, Stanchina ML, Malhotra A, et al. Effect of
increased lung volume on sleep disordered breathing in
patients with sleep apnoea. Thorax. 2006;61(5):435-439.
20. Hoffstein V, Zamel N, Phillipson EA. Lung volume dependence
of pharyngeal cross-sectional area in patients with obstructive
sleep apnea. Am Rev Respir Dis. 1984;130(2):175-178.
21. Sériès F, Cormier Y, Lampron N, La Forge J. Increasing the
functional residual capacity may reverse obstructive sleep
apnea. Sleep. 1988;11(4):349-353.
22. Wellman A, Malhotra A, Fogel RB, Edwards JK, Schory K,
White DP. Respiratory system loop gain in normal men and
women measured with proportional-assist ventilation. J Appl
Physiol. 2003;94(1):205-212.
23. Younes M. Role of arousals in the pathogenesis of obstructive sleep apnea. Am J Respir Crit Care Med. 2004;169(5):
623-633.
24. Gothe B, Bruce E, Goldman MD. Influence of sleep state on
respiratory muscle function. In: Saunders NA, Sullivan CE,
eds. Sleep and Breathing. New York, NY: Marcel Dekker,
Inc.; 1984:241-282.
25. White DP, Mezzanotte WS. Neuromuscular compensation in
the human upper airway. Sleep. 1993;16(8)(Suppl):S90-S91,
discussion S91-S92.
528
Diagnose
26. McGinley B, Halbauer A, Patil SP, et al. An open nasal cannula treats obstructive sleep apnea in children. Pediatrics.
2009;124(1):179-188.
27. Gold AR, Schwartz AR. The pharyngeal critical pressure. The
whys and hows of using nasal continuous positive airway pressure diagnostically. Chest. 1996;110(4):1077-1088.
28. Patil SP, Schneider H, Schwartz AR, Smith PL. Adult
obstructive sleep apnea: pathophysiology and diagnosis. Chest.
2007;132(1):325-337.
29. Dempsey JA, Skatrud JB. A sleep-induced apneic threshold
and its consequences. Am Rev Respir Dis. 1986;133(6):11631170.
30. Marcus CL. Sleep-disordered breathing in children. Am J
Respir Crit Care Med. 2001;164(1):16-30.
31. Guilleminault C. Obstructive sleep apnea syndrome and its
treatment in children: areas of agreement and controversy.
Pediatr Pulmonol. 1987;3(6):429-436.
32. Gold AR, Dipalo F, Gold MS, O’Hearn D. The symptoms
and signs of upper airway resistance syndrome: a link to the
functional somatic syndromes. Chest. 2003;123(1):87-95.
33. Gold AR, Dipalo F, Gold MS, Broderick J. Inspiratory airflow
dynamics during sleep in women with fibromyalgia. Sleep.
2004;27(3):459-466.
Original Research
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© 2010 American College of Chest Physicians
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Diagnose
Predictors for Treating Obstructive Sleep Apnea With an Open Nasal
Cannula System (Transnasal Insufflation)
Georg Nilius, Thomas Wessendorf, Joachim Maurer, Riccardo Stoohs,
Susheel P. Patil, Norman Schubert and Hartmut Schneider
Chest 2010;137; 521-528; Prepublished online December 1, 2009;
DOI 10.1378/chest.09-0357
This information is current as of April 13, 2010
Updated Information
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References
This article cites 31 articles, 16 of which can be
accessed free at:
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full.html#ref-list-1
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39
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Effect of a High-Flow Open Nasal Cannula System on Obstructive Sleep Apnea
in Children
Brian McGinley, Ann Halbower, Alan R. Schwartz, Philip L. Smith, Susheel P. Patil
and Hartmut Schneider
Pediatrics 2009;124;179-188
DOI: 10.1542/peds.2008-2824
The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://www.pediatrics.org/cgi/content/full/124/1/179
PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1948. PEDIATRICS is owned, published,
and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk
Grove Village, Illinois, 60007. Copyright © 2009 by the American Academy of Pediatrics. All
rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.
Downloaded from www.pediatrics.org at Welch Medical Library-Jhu on July 14, 2009
40
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ARTICLES
Effect of a High-Flow Open Nasal Cannula System on
Obstructive Sleep Apnea in Children
CONTRIBUTORS: Brian McGinley, MD,a Ann Halbower, MD,b Alan
R. Schwartz, MD,c Philip L. Smith, MD,c Susheel P. Patil, MD, PhD,c
and Hartmut Schneider, MD, PhDc
of Pediatric Pulmonology and cPulmonary and Critical
Care Medicine, Johns Hopkins Pediatric Sleep Disorders Center,
Johns Hopkins University, Baltimore, Maryland; bChildren’s
Hospital Pediatric Sleep Disorders Center, Division of Pediatric
Pulmonology, Children’s Hospital and University of Colorado,
Aurora, Colorado
aDivisions
KEY WORDS
pediatric obstructive sleep apnea, treatment of sleep apnea, TNI
ABBREVIATIONS
OSA— obstructive sleep apnea
CPAP— continuous positive airway pressure
TNI—treatment with nasal insufflation
REM—rapid eye movement
NREM—nonrapid eye movement
AHI—apnea-hypopnea index
www.pediatrics.org/cgi/doi/10.1542/peds.2008-2824
doi:10.1542/peds.2008-2824
Address correspondence to Brian McGinley, MD, Johns Hopkins
Department of Pediatrics, 200 North Wolfe St, Baltimore, MD
21287. E-mail: [email protected]
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).
Copyright © 2009 by the American Academy of Pediatrics
FINANCIAL DISCLOSURE: Dr Schneider received consulting fees
from TNI medical in 2006 and is entitled to royalty payments on
the future sales of products described in this article. Under a
separate licensing agreement between Dr Schneider and TNI
medical and Johns Hopkins University, Dr Schneider is entitled
to a share of royalty received by the university on sales of
products described in this article. The terms of this agreement
are being managed by Johns Hopkins University in accordance
with its conflict of interest policies. Dr Schneider was not
involved in the analysis of the study data, and data collected
under this study were masked with respect to patient identifiers
and clinical outcomes to Dr Schneider. The nonconflicted faculty
members were responsible for all of the data analysis. Funding
for the study described in this article was partially provided by
TNI medical.
WHAT’S KNOWN ON THIS SUBJECT: Adenotonsillectomy is the
treatment for children with sleep apnea. For children whom
surgery is not recommended or have residual sleep apnea after
surgery CPAP is recommended. CPAP, however, is encumbered by poor
adherence, leaving a large number of children untreated.
WHAT THIS STUDY ADDS: We present a novel treatment for sleep
apnea in children. Our data suggest that TNI may offer an
alternative to CPAP in some children. The minimally intrusive
interface of TNI may improve adherence to treatment.
abstract
OBJECTIVE: Obstructive sleep apnea syndrome in children is associated with significant morbidity. Continuous positive airway pressure
(CPAP) treats obstructive apnea in children, but is impeded by low
adherence. We, therefore, sought to assess the effect of warm humidified air delivered through an open nasal cannula (treatment with nasal insufflation [TNI]) on obstructive sleep apnea in children with and
without adenotonsillectomy.
METHODS: Twelve participants (age: 10 ⫾ 1 years; BMI: 35 ⫾ 14 kg/
m2), with obstructive apnea-hypopnea syndrome ranging from mild
to severe (2–36 events per hour) were administered 20 L/min of
air through a nasal cannula. Standard sleep architecture, sleepdisordered breathing, and arousal indexes were assessed at baseline,
on TNI, and on CPAP. Additional measures of the percentage of time
with inspiratory flow limitation, respiratory rate, and inspiratory duty
cycle were assessed at baseline and on TNI.
RESULTS: TNI reduced the amount of inspiratory flow limitation, which
led to a decrease in respiratory rate and inspiratory duty cycle. TNI
improved oxygen stores and decreased arousals, which decreased
the occurrence of obstructive apnea from 11 ⫾ 3 to 5 ⫾ 2 events per
hour (P ⬍ .01). In the majority of children, the reduction in the apneahypopnea index on TNI was comparable to that on CPAP.
CONCLUSIONS: TNI offers an alternative to therapy to CPAP in children
with mild-to-severe sleep apnea. Additional studies will be needed to
determine the efficacy of this novel form of therapy. Pediatrics 2009;
124:179–188
PEDIATRICS Volume 124, Number 1, July 2009
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179
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Obstructive sleep apnea (OSA) in children is attributed to upper airway collapse1–3 that is associated with intermittent hypoxemia, neurocognitive
dysfunction,4–8 and cardiovascular
morbidity.9–12 Moreover, recent data
suggest that milder degrees of obstructive sleep-disordered breathing
are associated with neurobehavioral
deficits,13,14 highlighting the social and
medical burdens of sleep-disordered
breathing in children.
Treatment of sleep apnea in children
includes both medical15 and surgical
options.16 Adenotonsillectomy is the
treatment of choice for the presence of
adenoid and tonsillar hypertrophy
with OSA. For children who are not suitable candidates for surgery, refuse adenotonsillectomy, or have residual
sleep apnea after surgical intervention, continuous positive airway pressure (CPAP)17 is the most effective
treatment option. CPAP, however, is encumbered by suboptimal adherence,18
leaving a large number of children untreated. Therefore, alternative therapeutic strategies to CPAP are required
to treat OSA in children more effectively. Recently, we demonstrated that
air delivered at a high flow rate
through a nasal cannula (treatment
with nasal insufflation [TNI]) alleviated
upper airway obstruction in adults
with OSA.19 Children with upper airway
obstruction during sleep, however, differ markedly with regard to the distribution of obstructive events. They have
obstructive apneas predominantly
during rapid eye movement (REM)
compared with nonrapid eye movement (NREM) sleep.20 In contrast to
adults, children commonly exhibit periods of prolonged stable partial upper
airway obstruction during sleep, including during NREM sleep.21 Thus,
whereas the rate of obstructive events
per hour of sleep (apnea-hypopnea index [AHI]) allows for quantification of
180
42
McGINLEY et al
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changes in upper airway obstruction
for REM sleep, other measures are
needed to assess upper airway obstruction during NREM sleep. It has
been demonstrated previously that the
inspiratory time relative to the duration of the respiratory cycle, the inspiratory duty cycle, increases linearly
with the degree of upper airway obstruction.22–24 Therefore, we determined the effect of TNI on upper airway
obstruction in children by assessing
both the AHI and the inspiratory duty
cycle. We hypothesized that TNI would
alleviate upper airway obstruction
during both REM and NREM sleep and
that, in a significant proportion of children, improvements in the AHI would
be similar to CPAP.
PATIENTS AND METHODS
Study Population
Children 5 to 15 years of age were recruited consecutively from the Johns
Hopkins Pediatric Sleep Disorders
Center if they had OSA and were recommended treatment with CPAP. Patients were excluded if they had a nocturnal oxygen requirement or other
serious medical conditions. Informed
consent was obtained from 1 parent or
guardian, assent was obtained from
the children, and the Johns Hopkins
Medicine Institutional Review Board
approved the protocol.
Protocols
Each participant underwent 2 overnight polysomnograms, 1 with TNI at 20
L/min and 1 night off TNI, performed in
random order. For children who had
participated in a clinical CPAP titration
study before enrollment, that study
was analyzed to compare the AHI between TNI and CPAP at the prescribed
nasal pressure level. Children continued home use of CPAP while enrolled in
the study.
Study Materials
Polysomnography
Sleep studies were performed with
Somnologica (Embla, Broomfield, CO).
Signals included electroencephalograms (leads C3-A2, C4-A1, and O1-A2),
left and right electro-oculograms, submental electromyogram, tibial electromyogram, electrocardiogram, and
oxyhemoglobin saturation (Masimo, Irvine, CA). End-tidal CO2 (Novametrix,
Murrysville, PA) was acquired from all
of the participants during the baseline
night, but the signal could not be obtained during the treatment night because of interference from TNI. Transcutaneous CO2 measurement (TCM3,
Radiometer Kopenhagen, Copenhagen,
Denmark) was acquired in 5 participants during the baseline and in 3 of
those subjects during the treatment
night with TNI. Airflow measurement
was acquired with a nasal cannula
(Salter Labs, Arvin, CA) connected to a
differential pressure transducer (ProTech, Mukilteo, WA). Respiratory effort
was assessed with thoracic and abdominal inductive plethysmography
(Embla), and body position was monitored via infrared video camera.
To ensure that the airflow signals acquired from the nasal cannula were
not affected by TNI, preliminary studies
were conducted comparing the qualitative airflow signals from a nasal cannula with those acquired concurrently
from a nasal mask attached to a pneumotachograph while TNI was turned
on and off during sleep. The contour
and amplitude of the airflow signal acquired from the nasal cannula were
consistently similar to those of the nasal mask when TNI was turned on and
off, indicating that TNI did not interfere
with our ability to detect inspiratory
flow limitation (see Fig 1).
Nasal Insufflation (TNI)
An air compressor (TNI Medical GmbH,
Heilbronn, Germany) delivered a con-
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ARTICLES
FIGURE 1
Qualitative airflow signals from a nasal mask attached to a pneumotachograph compared with those acquired concurrently from a nasal cannula attached
to a pressure transducer during TNI trials are depicted. Changes in baseline airflow in the nasal cannula at the onset and offset of TNI are attributed to an
alternating current-coupled signal with a long time constant.
stant flow rate at the level of the nasal
prongs of the TNI cannula at a maximum of 20 L/min. A heater and humidifier regulated the temperature and
humidity. A heated wire incorporated
into the lumen of the nasal cannula
maintained a temperature of 30°C to
33°C and a relative humidity of ⬃80%
at the nasal outlet (Fig 2).
Analysis
Sleep and Respiratory Events
Standard polysomnographic scoring
techniques were used to stage sleep,
arousals, and respiratory events.25 An
AHI was calculated for obstructive and
central respiratory events per hour of
sleep separately for each individual
for the entire night and for NREM and
REM sleep. Because the primary outPEDIATRICS Volume 124, Number 1, July 2009
come was effect on upper airway obstruction, AHI data pertain specifically
to obstructive events. If REM sleep time
was ⬍20 minutes on either the baseline or TNI treatment night, the participant was excluded from the analysis
of REM AHI.
Respiratory Pattern
Children
with
sleep-disordered
breathing commonly exhibit apneic
events during REM as compared with
NREM sleep.20 Thus, upper airway obstruction during NREM sleep was also
assessed by the following: percentage
of time with flow-limited breathing, inspiratory duty cycle (length of the inspiratory time divided by length of the
respiratory cycle), and respiratory
rate for the baseline and TNI-treatment
nights. Inspiratory flow limitation was
assessed by visual inspection, as described previously,26–29 and quantified
as the percentage of NREM sleep time
that it was exhibited. A custom computer program that randomly generated two 3-minute samples per hour of
NREM sleep determined breaths analyzed. All of the breaths in each sample
were included in the analysis irrespective of the presence or absence of inspiratory flow limitation.
Statistical Analysis
Data are reported as the means ⫾
SEMs. The Wilcoxon sign-rank test was
performed (Stata 8, Stata Corp, College Station, TX) to compare differences in sleep architecture, arousal
indexes, oxyhemoglobin saturation,
and measures of sleep-disordered
breathing between the baseline and
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FIGURE 2
One study participant wearing the TNI cannula (left) and the TNI device is depicted (right). Cannula length is 1800.0 mm, outer diameter 5.0-mm cannula and
nasal prongs, and inner diameter 3.4 mm. The weight of the TNI device including the compressor is ⬃10 kg.
TNI-treatment nights. P values of ⬍.05
were considered significant.
RESULTS
Participant Characteristics
Twelve otherwise healthy children with
sleep apnea aged 10 ⫾ 2 years were
enrolled. The majority of children were
boys and obese (Table 1). Selfreported CPAP use was for ⬍4 hours
per night and ⬍5 days per week in half
of the children. Although these adherence rates are consistent with previ-
ous studies of CPAP use,18 most children in this study were ineffectively
treated.
Polysomnographic Responses to TNI
Sleep-Disordered Breathing Events
In Fig 3, the effect of TNI on sleepdisordered breathing is illustrated in
1 child (child No. 7). In this child, obstructive hypopneas were observed
primarily during REM sleep without TNI
treatment (Fig 2, top left). Each hypop-
nea was characterized by decreased
inspiratory airflow and a small reduction in oxyhemoglobin saturation and
was terminated by a cortical arousal
from sleep. The last 4 breaths of each
hypopnea had a flattened inspiratory
flow contour with increasing inspiratory effort, indicating that these events
were obstructive hypopneas. In contrast, on TNI (Fig 2, top right), hypopneas were abolished, leading to a stabilization of sleep and oxyhemoglobin
saturation (Table 2).
TABLE 1 Patient Anthropometrics and Characteristics
Patient ID No.
Anthropometrics
Gender
Age, y
Height, cm
Weight, kg
BMI, kg/m2
BMI z score
Previous treatment
CPAP, cm H2O
Adenotonsillectomy
Disordered breathing indexes
AHI total, events per hour
SPO2 nadir, %
Peak CO2, mm Hg
% TST CO2 ⬎50 mm Hg
Daytime symptoms
1
2
3
F
8
142
53
26
2.2
M
13
159
72
28
1.9
M
10
137
75
40
2.7
11
⫹
8
⫹
7
⫹
2
90
51
0.1
DS, H
2
92
50
0
H, IC
2
96
53
1
H, IC, BD
4
5
6
7
M
7
127
22
14
⫺1.5
M
9
125
25
16
⫺0.1
M
11
153
92
36
2.7
M
9
141
54
27
2.2
NA
⫺
7
⫹
8
⫺
5
87
60
52
DS, H
8
90
53
1
None
3
95
54
3
H, IC, BD
8
9
10
11
12
F
F
F
14
14
12
165 161 177
129 116 132
47
45
42
2.8
2.8
1.5
Mean
SEM
8 M/4 F
10
145
75
35
1.6
—
1
5
12
4
0.4
M
10
159
134
53
2.9
M
10
161
50
19
1.1
10
⫹
5
⫺
7
⫺
20
⫹
5
⫹
NA
⫹
9
8⫹/4⫺
1
—
9
88
59
37
H, IC
9
84
58
5
DS, BD
17
94
55
1
H, IC, BD
20
79
54
7
DS
22
83
56
7
DS
36
68
63
56
H, BD
11
87
56
14
—
3
2
1
6
—
SPO2 nadir indicates oxyhemoglobin saturation; CO2 indicates end-tidal CO2; % TST CO2 ⬎50 mm Hg, percentage of total sleep time that CO2 was ⬎50 mm Hg; DS, daytime sleepiness; H,
hyperactivity; IC, impaired concentration; BD, behavior disorder; M, male; F, female; —, no data; NA, not applicable.
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TABLE 2 Sleep Efficiency and Stage Data Are Presented as the Percentage of Time/Total Sleep Time
Variable
Sleep architecture
Total sleep time, min
Sleep efficiency, %
Stage N1, %
Stage N2, %
Stage N3, %
Stage R, %
Arousal indexes, events per hour of sleep
Total
Respiratory
Spontaneous
Oxyhemoglobin saturation
Average during sleep, %
Average desaturation, %
Desaturation nadir, %
Similar responses were observed in
the total AHI during the baseline compared with treatment with TNI, respectively (11 ⫾ 3 vs 5 ⫾ 2 events per hour)
Baseline,
Mean ⫾ SEM
TNI,
Mean ⫾ SEM
P
296.6 ⫾ 14.3
91.3 ⫾ 2.7
3.2 ⫾ 0.8
48.1 ⫾ 3.1
21.3 ⫾ 3.7
16.2 ⫾ 3.1
284.9 ⫾ 16.3
86.2 ⫾ 4.3
5.2 ⫾ 1.4
51.1 ⫾ 2.9
20.9 ⫾ 2.6
14.7 ⫾ 2.2
.07
.04
.2
.4
.9
.7
13.9 ⫾ 1.6
8.0 ⫾ 1.9
5.9 ⫾ 0.6
10.1 ⫾ 1.7
4.1 ⫾ 1.5
5.9 ⫾ 0.8
.05
.02
.8
98.0 ⫾ 1.0
5.0 ⫾ 1.0
88.0 ⫾ 2.0
98.0 ⫾ 1.0
3.0 ⫾ 1.0
93.0 ⫾ 1.0
.7
.02
.01
in nearly all of the children (Fig 4,
right). Subanalyses were performed
separately for REM and NREM sleep to
assess the effect of sleep stage on the
response to TNI. Four participants
were excluded from the REM analysis
because they did not have sufficient
REM sleep time during the TNI treatment night, leaving 8 participants (boy:
girl ratio: 7:1). During TNI treatment,
the AHI was markedly reduced during
both NREM from 8 ⫾ 3 to 4 ⫾ 2 events
per hour (Fig 4, left) and REM sleep
from 26 ⫾ 10 to 11 ⫾ 5 events per hour
(Fig 4, middle). Central apnea rates
were minimal (0.1 ⫾ 0.1 and 0.3 ⫾ 0.2
events per hour) during the baseline
and TNI study nights, respectively. The
effect of body position on the response
was also assessed. During the baseline compared with the treatment
night with TNI, respectively, the mean
percentages of sleep time in the supine (78.0% ⫾ 8.4% vs 79.0% ⫾ 9.5%;
FIGURE 3
Two hypoponeas during REM sleep at baseline are shown (top left), which are abolished on TNI (top right). During NREM sleep, the same child exhibited
inspiratory flow limitation characterized by plateauing of the inspiratory contour (bottom left), which was alleviated with TNI (bottom right). EOG indicates
electrooculogram; EEG, electroencephalogram; SpO2, oxyhemoglobin saturation. RR indicates respiratory rate.
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P ⫽ .5) and side or prone body positions (22.0% ⫾ 8.4% vs 21.0% ⫾ 9.5%;
P ⫽ .5) were comparable, but there
were differences in 4 participants.
Analysis of the AHI in these 4 children
was performed while they were in a
supine position only, and a greater decline in the AHI was observed with TNI
treatment, indicating that changes in
body position did not account for the
reduction in the AHI observed on TNI
treatment. Of note, polysomnographic
responses were comparable in children with and without adenotonsillectomy (Fig 4).
mean prescribed nasal pressure was
9 ⫾ 4 cm H2O (Table 1). The AHI on TNI
treatment compared with CPAP treatment was 5 ⫾ 2 vs 1 ⫾ 1 events per
hour (P ⫽ .08). As compared with
CPAP, 2 children had suboptimal responses on TNI treatment (participant
No. 10 and No. 11; Fig 4, denoted by b).
Both of these children had severe
sleep apnea (AHI ⬎20 events per
hour); 1 required a CPAP pressure of
20 cm H2O to alleviate upper airway
obstruction and the other did not tolerate either the CPAP mask or the TNI
device, which resulted in significant
sleep disruption on both study nights.
In the remaining children (n ⫽ 8), the
AHI on TNI treatment compared with
CPAP treatment was 2 ⫾ 1 vs 1 ⫾ 1
event per hour, indicating that, for the
majority of children, treatment with
TNI was comparable clinically to CPAP
treatment.
Sleep
Between the baseline and treatment
with TNI nights, total sleep time and
sleep stage distribution were similar,
but we observed a slight decrease in
sleep efficiency. The total and respiratory arousal indexes also decreased
during the night of treatment with TNI,
but the spontaneous arousal index
was similar (Table 2).
Respiratory Pattern Responses to
TNI
Comparison With CPAP
Sleep-disordered breathing in our
study population was generally characterized by apneic events during REM
Ten of the 12 children had undergone
CPAP titration before this study. The
REM
NREM
Total
(n = 8)
(n = 12)
(n = 12)
80
P < .01
P = .01
P < .01
AHI, events per h
60
40
a
a
a
20
b
b
0
Baseline
TNI
Baseline
TNI
Baseline
TNI
FIGURE 4
The AHIs are displayed for the baseline compared with the TNI-treatment night during NREM (left), REM
(middle), and for the entire night (right). Data presented are means ⫾ SEMs. a Participants with
residual sleep apnea on TNI. b Participants with suboptimal AHI responses on TNI compared with CPAP.
䡩 Children without adenotonsillectomy.
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sleep and prolonged periods of steadystate inspiratory flow limitation during
NREM sleep. During the baseline study
off of TNI treatment, the periods of inspiratory flow limitation were associated with elevations in respiratory
rate and inspiratory duty cycle (Fig 2,
bottom left). TNI reduced the amount of
inspiratory flow limitation, which resulted in a decreased respiratory rate
and inspiratory duty cycle (Fig 2, bottom right). Mean data for all of the participants during NREM sleep demonstrated that TNI reduced the amount of
inspiratory flow limitation, which was
associated with a decrease in both the
inspiratory duty cycle and the respiratory rate (Fig 5).
DISCUSSION
There were 3 major findings in our
study of TNI. First, in a group of predominantly obese children with and
without adenotonsillectomy, TNI treated
sleep apnea across a wide spectrum of
disease severity. Second, in the majority of children, the reduction in the AHI
with TNI was comparable to CPAP.
Third, during NREM sleep, all of the
children had prolonged periods of inspiratory flow limitation that were associated with an increased respiratory
rate and inspiratory duty cycle, all of
which decreased with TNI. Our data
suggest that TNI may offer an alternative to CPAP in some children for whom
standard treatment approaches are
not successful.
Previously, we demonstrated that TNI
treated all of the adult participants
with mild sleep apnea and approximately half of the adult participants
with moderate and severe sleep apnea.19 Children in the current study
were equally distributed across a
spectrum of disease severity (mild AHI:
⬎2 and ⱕ5 events per hour, n ⫽ 4;
moderate AHI: ⬎5 and ⱕ10 events per
hour, n ⫽ 4; and severe AHI: ⬎10
events per hour, n ⫽ 4). TNI reduced
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Inspiratory flow limitation
0.80
100
35
P < .01
P < .01
P < .01
0.70
60
40
20
30
Breaths per min
Inspiratory time/respiratory cycle time
80
% of NREM sleep time
Respiratory rate
Inspiratory duty cycle
0.60
0.50
0.40
TNI
Off
TNI
On
20
15
0.30
0
25
10
TNI
Off
TNI
On
TNI
Off
TNI
On
FIGURE 5
Graphic representations of the respiratory pattern during NREM sleep for the baseline compared with
TNI: percentage of NREM sleep time with inspiratory flow limitation (left); inspiratory duty cycle, which
is the inspiratory time/duration of the respiratory cycle (middle); and respiratory rate (right). Data
presented are means ⫾ SEMs.
the AHI during both NREM and REM
sleep, but this effect depended on the
disease severity. In the 8 children with
mild-to-moderate sleep apnea, TNI decreased the AHI consistently, with a
mean reduction from 6 ⫾ 3 to 2 ⫾ 1
events per hour. In contrast, in the 4
children with severe sleep apnea, TNI
had an inconsistent response: in 1
child, the AHI was unchanged, in 2 children the AHI decreased by 72% and
36% but the effect was suboptimal, and
the fourth child had a marked reduction in the AHI from 17 to 2 events per
hour. The 3 children whose AHI remained above 10 events per hour (Fig
4) were unique in the following aspects: they were all girls, markedly
obese, and were in Tanner stage 2 to 3
as compared with the other children,
who were generally younger and in
Tanner stage 1. Thus, TNI might offer a
treatment option for children with
mild-to-moderate OSA and in selected
children with severe OSA.
OSA is the result of increased upper
airway collapsibility during sleep, as
reflected in the critical closing presPEDIATRICS Volume 124, Number 1, July 2009
sure.2,3,30–33 Previously, we demonstrated that TNI primarily acts by
slightly increasing pharyngeal pressure19 that was particularly effective in
adults with minimal increases in critical closing pressure manifested clinically by snoring and hypopneas.34 Similarly, TNI alleviated inspiratory flow
limitation during NREM sleep (Fig 4).
The marked reduction in apneic events
during REM sleep, however, was
greater than anticipated. This finding
suggests that TNI might have increased pharyngeal pressure more in
children than adults because of the
relatively larger size of the nasal cannula compared with the size of the nares. Alternatively, the slight increase in
pharyngeal pressure might have increased lung volume to a greater degree in children resulting from higher
chest wall and lung compliance,35 particularly during REM sleep, when the
chest wall musculature is hypotonic.36
Increases in lung volume might have
improved both oxygen stores and upper airway patency.37–40 Finally, it is
also possible that insufflation of air
might have stimulated upper airway
neuromuscular responses, thereby
improving upper airway patency.41 Regardless, the improvements in flow
limitation, respiratory rate, and inspiratory duty cycle suggest that TNI
increased inspiratory tidal volumes
through increased inspiratory airflow.
Moreover, the improvement in the AHI
with TNI suggests that the increases in
inspiratory airflow and tidal volumes
were sufficient to prevent hypoxia or
arousals, which has significant implications for the management of sleepdisordered breathing in children.
There are several advantages of TNI.
First, the patient interface is a nasal
cannula that is less cumbersome than
a nasal mask and should be better tolerated by children during sleep. All of
the participants readily agreed to
sleep with a TNI device, and only 2 participants described mild discomfort
once the TNI device began to deliver
air. One complaint was temperature
related and was easily adjusted to the
participant’s preference; 1 participant
intermittently removed the cannula
during the course of the night but was
unable to effectively verbalize her complaint. Second, TNI delivers heated and
humidified air at the level of the nares,
which avoids nasal dryness and irritation. Third, for the majority of children,
the response to TNI was comparable to
CPAP. Taken together, if improved comfort with TNI leads to increased adherence to treatment, TNI might ultimately
be a more effective treatment option
than CPAP, even in children with suboptimal responses. To assess this hypothesis, however, adherence with TNI
needs to be assessed in the home setting. Fourth, the use of CPAP in children
carries concern for the potential of
compression of boney facial structures. TNI is an open system that is not
dependent on a tightly sealed nasal
mask obviating concerns of facial
compression.
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There were several limitations in our
study. First, carbon dioxide levels were
evaluated during the baseline study,
but the high airflow rate of TNI eliminated the end-tidal CO2 measurement
during the treatment night. The loss of
a consistent CO2 measurement limited
our ability to assess the effect of TNI on
ventilation during the treatment night.
Second, the sample size was limited,
and the effect of TNI on severe sleep
apnea is not completely understood.
The spectrum of patients with regard
to disease severity and previous adenotonsillectomy, however, was diverse and likely representative of patients who would require treatment
for sleep apnea. Third, the total sleep
times during both nights were limited
because of testing conditions, which
included an early awakening time. Additional evaluation of the effect of TNI
on sleep time, sleep latency, and sleep
architecture should be assessed in future studies. Fourth, the assessment of
Diagnose
respiratory pattern changes during
NREM sleep with TNI was measured
with a random sample of breaths. It is
possible that the changes observed in
the respiratory pattern on TNI might
have been more accurately characterized if the assessment was expanded
to include all breaths during NREM
sleep.
CONCLUSIONS
Adenotonsillectomy continues to be
the treatment of choice for children
with sleep apnea.16,42,43 The reduction
in the AHI with TNI was comparable in
children with and without adenotonsillectomy, indicating that TNI is a treatment option for children awaiting adenotonsillectomy and for those with
residual sleep apnea after adenotonsillectomy (Fig 4). Moreover, there is
significant controversy regarding
which children with milder degrees of
sleep-disordered breathing might benefit from treatment.15,44 The effect of
TNI on sleep-disordered breathing in-
dicates that TNI might provide an alternative to surgery and, as compared
with CPAP, might be a more readily accepted treatment option.
The minimally intrusive nasal interface
of TNI may improve adherence to treatment in children and may ultimately
prove more effective in managing the
long-term morbidity and mortality of
sleep apnea. Additional studies will be
required to extend these findings to
additional pediatric populations, including younger children and infants
and those children with neuromuscular or craniofacial disorders, to determine the ultimate role for TNI in
the management of sleep-disordered
breathing in children.
ACKNOWLEDGMENTS
This study was funded by National
Heart, Lung, and Blood Institute grants
HL-72126, HL-50381, HL-37379, and HL077137 and National Health and Medical Research Council grant 353705.
REFERENCES
1. Eastwood PR, Szollosi I, Platt PR, Hillman DR. Comparison of upper airway collapse during general
anesthesia and sleep. Lancet. 2002;359(9313):1207–1209
2. Schwartz AR, Smith PL, Wise RA, Gold AR, Permutt S. Induction of upper airway occlusion in
sleeping individuals with subatmospheric nasal pressure. J Appl Physiol. 1988;64(4):535–542
3. Smith PL, Wise RA, Gold AR, Schwartz AR, Permutt S. Upper airway pressure-flow relationships in
obstructive sleep apnea. J Appl Physiol. 1988;64(2):789 –795
4. Chervin RD, Archbold KH. Hyperactivity and polysomnographic findings in children evaluated for
sleep-disordered breathing. Sleep. 2001;24(3):313–320
5. Owens J, Opipari L, Nobile C, Spirito A. Sleep and daytime behavior in children with obstructive
sleep apnea and behavioral sleep disorders. Pediatrics. 1998;102(5):1178 –1184
6. Weissbluth M, Davis A, Poncher J, Reiff J. Signs of airway obstruction during sleep and behavioral,
developmental and academic problems. J Dev Behav Pediar. 1983;4(2):119 –121
7. Halbower AC, Degaonkar M, Barker PB, Earley CJ, Marcus CL, Smith PL. Childhood obstructive
sleep apnea associates with neuropsychological deficits and neuronal brain injury. PLoS Med.
2006;3(8):e301
8. Gozal D. Sleep-disordered breathing and school performance in children. Pediatrics. 1998;102(3
pt 1):616 – 620
9. Amin RS, Carroll JL, Jeffries JL, Grone C, Bean JA, Chini B. Twenty-four-hour ambulatory blood
pressure in children with sleep-disordered breathing. Am J Respir Crit Care Med. 2004;169(8):
950 –956
10. Enright PL, Goodwin JL, Sherrill DL, Quan JR, Quan SF. Blood pressure elevation associated with
sleep-related breathing disorder in a community sample of white and Hispanic children: the
Tucson Children’s Assessment of Sleep Apnea Study. Arch Pediatr Adolesc Med. 2003;157(9):
901–904
11. Marcus CL, Greene MG, Carroll JL. Blood pressure in children with obstructive sleep apnea. Am J
Respir Crit Care Med. 1998;57(4 pt 1):1098 –1103
186
48
McGINLEY et al
Downloaded from www.pediatrics.org at Welch Medical Library-Jhu on July 14, 2009
Therapie
TNI® Studien
Diagnose
ARTICLES
12. Quan SF, Gersh BJ. Cardiovascular consequences of sleep-disordered breathing: past, present
and future: report of a workshop from the National Center on Sleep Disorders Research and the
National Heart, Lung, and Blood Institute. Circulation. 2004;109(8):951–957
13. Blunden S, Lushington K, Lorenzen B, Martin J, Kennedy D. Neuropsychological and psychosocial
function in children with a history of snoring or behavioral sleep problems. J Pediatrics. 2004;
146(6):780 –786
14. O’Brien LM, Mervis CB, Holbrook CR, Bruner JL, Klaus CJ, Rutherford J. Neurobehavioral implications of habitual snoring in children. Pediatrics. 2004;114(1):44 – 49
15. Kheirandish-Gozal L, Gozal D. Intranasal budesonide treatment for children with mild obstructive
sleep apnea syndrome. Pediatrics. 2008;122(1). Available at: www.pediatrics.org/cgi/content/full/
122/1/e149
16. Guilleminault C, Li K, Khramtsov A, Pelayo R, Martinez S. Sleep disordered breathing: surgical
outcomes in prepubertal children. Laryngoscope. 2004;114(1):132–137
17. Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous
positive airway pressure applied through the nares. Lancet. 1981;1(8225):862– 865
18. Marcus CL, Rosen G, Ward S, Halbower AC, Halbower AC, Sterni L, Lutz J. Adherence to and
effectiveness of positive airway pressure therapy in children with obstructive sleep apnea. Pediatrics. 2006;117(3). Available at: www.pediatrics.org/cgi/content/full/117/3/e442
19. McGinley BM, Patil SP, Kirkness JP, Smith PL, Schwartz AR, Schneider H. A nasal cannula can be
used to treat obstructive sleep apnea. Am J Respir Crit Care Med. 2007;176(2):194 –200
20. Goh DY, Galster P, Marcus CL. Sleep architecture and respiratory disturbances in children with
obstructive sleep apnea. Am J Respir Crit Care Med. 2000;162(pt 2):682– 686
21. Marcus CL. Obstructive sleep apnea syndrome: differences between children and adults. Sleep.
2000;23(suppl 4):S140 –S141
22. Marcus CL, Moreira GA, Bamford O, Lutz J. Response to inspiratory resistive loading during sleep
in normal children and children with obstructive apnea. J Appl Physiol. 1999;87(4):1448 –1454
23. Badr M S, Skatrud JB, Dempsey JA, Begle RL. Effect of mechanical loading on expiratory and
inspiratory muscle activity during NREM sleep. J Appl Physiol. 1990;68(3):1195–1202
24. Schneider H, Patil SP, Canisius S, Gladmon EA, Schwartz AR, O’Donnell CP. Hypercapnic duty cycle
is an intermediate physiological phenotype linked to mouse chromosome 5. J Appl Physiol. 2003;
95(1):11–19
25. Iber C, Ancoli-Israel S, Chesson A Jr, Quan S, eds. The AASM Manual for the Scoring of Sleep and
Associated Events Rules, Terminology and Technical Specifications, 1st edition. Westchester, IL:
American Academy of Sleep Medicine; 2007
26. Ayappa I, Norman RG, Krieger A, Rosen A, O’malley RL, Rapoport DM. Non-invasive detection of
respiratory effort-related arousals (RERAS) by a nasal cannula/pressure transducer system.
Sleep. 2000;23(6):763–771
27. Hosselet JJ, Norman RG, Ayappa I, Rapoport DM. Detection of flow limitation with a nasal cannula/
pressure transducer system. Am J Respir Crit Care Med. 1998;157(5 pt 1):1461–1467
28. Serebrisky D, Cordero R, Mandeli J, Kattan M, Lamm C. Assessment of inspiratory flow limitation
in children with sleep-disordered breathing by a nasal cannula pressure transducer system.
Pediatr Pulmonlol. 2002;33(5):380 –387
29. Pichard LE, Patil SP, Gladmon E, Smith PL, Schwartz AR, Schneider H. Women have a greater
ventilatory responses to upper airway obstruction than men. Conf Proc IEEE Eng Med Biol Soc.
2004;5:3878 –3880
30. Boudewyns A, Punjabi N, Van de Heyning PH, DeBacker WA, O’Donnell CP, Scheider H. Abbreviated
method for assessing upper airway function in obstructive sleep apnea. Chest. 2000;118(4):
1031–1041
31. Issa FG, Sullivan CE. Upper airway closing pressures in obstructive sleep apnea. J Appl Physiol.
1984;57(2):520 –527
32. Marcus CL, Katz ES, Lutz J, Black CA, Galster P, Carson KA. Upper airway dynamic responses in
children with the obstructive sleep apnea syndrome. Pediatr Res. 2005;57(1):99 –107
33. Marcus CL, Fernandes Do, Prado LB, Lutz J, Katz ES, Black CA. Developmental changes in upper
airway dynamics. J Appl Physiol. 2004;97(1):98 –108
34. Gleadhill IC, Schwartz AR, Schubert N, Wise RA, Permutt S, Smith PL. Upper airway collapsibility in
snorers and in patients with obstructive hypopnea and apnea. Am Rev Respir Dis. 1991;143(6):
1300 –1303
35. Papastamelos C, Panitch HB, England SE, Allen JL. Developmental changes in chest wall compliance in infancy and early childhood. J Appl Physiol. 1995;78(1):179 –184
36. Tabachnik E, Muller NL, Bryan AC, Levison H. Changes in ventilation and chest wall mechanics
during sleep in normal adolescents. J Appl Physiol. 1981;51(3):557–564
PEDIATRICS Volume 124, Number 1, July 2009
Downloaded from www.pediatrics.org at Welch Medical Library-Jhu on July 14, 2009
187
49
Therapie
TNI® Studien
Diagnose
37. Heinzer RC, Stanchina ML, Malhotra A, Jordan AS, Patel SR, Lo YL. Effect of increased lung volume
on sleep disordered breathing in patients with sleep apnoea. Thorax. 2006;61(5):435– 439
38. Hoffstein V, Zamel N, Phillipson EA. Lung volume dependence of pharyngeal cross-sectional area in
patients with obstructive sleep apnea. Am Rev Respir Dis. 1984;130(2):175–178
39. Series F, Cormier Y, Desmeules M. Influence of passive changes of lung volume on upper airways.
J Appl Physiol. 1990;98(5):2159 –2164
40. Series F, Cormier Y, Lampron N, La Forge J. Increasing the functional residual capacity may
reverse obstructive sleep apnea. Sleep. 1988:11(4):349 –353
41. McGinley BM, Schwartz AR, Schneider H, Kirkness JP, Smith PL, Patil SP. Upper airway neuromuscular compensation during sleep is defective in obstructive sleep apnea. J Appl Physiol. 2008;
105(1):197–205
42. Stradling JR, Thomas G, Warley AR, Williams P, Freeland A. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and symptoms in snoring children. Lancet. 1990;335(8684):
249 –253
43. Section on Pediatric Pulmonology and Subcommittee on Obstructive Sleep Apnea Syndrome,
American Academy of Pediatrics. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109(4):704 –712
44. Sans Capdevila O, Kheirandish-Gozal L, Gozal D. Pediatric obstructive sleep apnea. complications,
management, and long-term outcomes. Proc Am Thoracic Soc. 2008;5(2):274 –282
188
50
McGINLEY et al
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Therapie
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Effect of a High-Flow Open Nasal Cannula System on Obstructive Sleep Apnea
in Children
Brian McGinley, Ann Halbower, Alan R. Schwartz, Philip L. Smith, Susheel P. Patil
and Hartmut Schneider
Pediatrics 2009;124;179-188
DOI: 10.1542/peds.2008-2824
Updated Information
& Services
including high-resolution figures, can be found at:
http://www.pediatrics.org/cgi/content/full/124/1/179
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51
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A Nasal Cannula Can Be Used to Treat Obstructive
Sleep Apnea
Brian M. McGinley1, Susheel P. Patil1, Jason P. Kirkness1, Philip L. Smith1, Alan R. Schwartz1, and
Hartmut Schneider1
1
Johns Hopkins Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Rationale: Obstructive sleep apnea syndrome is due to upper airway
obstruction and is associated with increased morbidity. Although
continuous positive airway pressure efficaciously treats obstructive
apneas and hypopneas, treatment is impeded by low adherence
rates.
Objectives: To assess the efficacy on obstructive sleep apnea of a
minimally intrusive method for delivering warm and humidified air
through an open nasal cannula.
Methods: Eleven subjects (age, 49.7 ⴞ 5.0 yr; body mass index, 30.5 ⴞ
4.3 kg/m2), with obstructive apnea–hypopnea syndrome ranging
from mild to severe (5 to 60 events/h), were administered warm
and humidified air at 20 L/minute through an open nasal cannula.
Measurements and Main Results: Measurements were based on standard sleep-disordered breathing and arousal indices. In a subset
of patients pharyngeal pressure and ventilation were assessed to
determine the mechanism of action of treatment with nasal insufflation. Treatment with nasal insufflation reduced the mean apnea–
hypopnea index from 28 ⴞ 5 to 10 ⴞ 3 events per hour (p ⬍ 0.01),
and reduced the respiratory arousal index from 18 ⴞ 2 to 8 ⴞ 2
events per hour (p ⬍ 0.01). Treatment with nasal insufflation reduced the apnea–hypopnea index to fewer than 10 events per hour
in 8 of 11 subjects, and to fewer than 5 events per hour in 4 subjects.
The mechanism of action appears to be through an increase in
end-expiratory pharyngeal pressure, which alleviated upper airway
obstruction and improved ventilation.
Conclusions: Our findings demonstrate clinical proof of concept that
a nasal cannula for insufflating high airflows can be used to treat
a diverse group of patients with obstructive sleep apnea.
Keywords: treatment with nasal insufflation, TNI; pharyngeal pressure
Obstructive sleep apnea syndrome is due to upper airway obstruction leading to intermittent hypoxemia, sleep fragmentation, metabolic dysfunction (1, 2), and increased cardiovascular
morbidity and mortality (3, 4). Current treatment options, including continuous positive airway pressure (5), oral appliances
(6), and surgical procedures (7), are often intrusive or invasive,
and not well tolerated, leaving a vast number of subjects untreated (8, 9). Therefore, improved therapeutic strategies are
required to treat sleep apneas and hypopneas and their associated morbidity and mortality.
Upper airway obstruction is due to increased pharyngeal collapsibility (10–12), which decreases inspiratory airflow as manifested by snoring and obstructive hypopneas and apneas (13).
This defect in upper airway collapsibility can be overcome by
elevating nasal pressure. In fact, somewhat greater levels of nasal
(Received in original form September 18, 2006; accepted in final form March 14, 2007 )
Supported by HL-72126, HL-50381, HL-37379, HL-077137, NHMRC-353705,
and Seleon GmbH, Germany.
Correspondence and requests for reprints should be addressed to Hartmut
Schneider, M.D., Ph.D., Johns Hopkins Asthma and Allergy Center, 5501 Hopkins
Bayview Circle, Room 4B47, Baltimore, MD 21224. E-mail: [email protected]
Am J Respir Crit Care Med Vol 176. pp 194–200, 2007
Originally Published in Press as DOI: 10.1164/rccm.200609-1336OC on March 15, 2007
Internet address: www.atsjournals.org
52
AT A GLANCE COMMENTARY
Scientific Knowledge on the Subject
High levels of continuous positive airway pressure (CPAP)
are needed to alleviate obstructive apneas; low compliance
with CPAP impedes its therapeutic effectiveness; and, because hypopneas can be treated with low levels of CPAP,
nasal insufflation of air might effectively treat mild obstructive sleep apnea.
What This Study Adds to the Field
Nasal insufflation can provide distinct clinical advantages
over CPAP for a substantial proportion of the patient population with sleep apnea.
pressure are required to abolish apneas than hypopneas, and
to restore normal levels of inspiratory airflow (12, 14). Thus,
minimally intrusive methods for delivering low levels of airway
pressure may be remarkably effective in treating hypopneas.
At present, continuous positive airway pressure (CPAP) is
most effective in eliminating apneas and hypopneas, although
long-term effectiveness is compromised by low adherence that
is estimated at only 50 to 60% (15, 16). Poor adherence has
been attributed to the side effects associated with nasal CPAP,
including difficulty tolerating pressure and the nasal mask interface, nasal irritation, claustrophobia, and skin breakdown (17,
18). To address these issues, we developed a simplified method
for increasing pharyngeal pressure by delivering warm and humidified air at a continuous high flow rate through an open nasal
cannula. The present study was designed to determine whether
treatment with nasal insufflation (TNI) alleviates obstructive
sleep apnea and hypopnea across a spectrum of disease severity.
Some of the results of these studies have been previously reported in the form of abstracts (19, 20).
METHODS
Participants
Subjects were recruited from the Johns Hopkins Sleep Disorders Center
(Johns Hopkins University, Baltimore, MD) if they had more than
five obstructive disordered breathing episodes per hour of sleep on a
standard overnight polysomnogram. Patients were selected to provide
a balanced range of disease severity encompassing a spectrum of mild
(apnea–hypopnea index [AHI] ⭓ 5–15 events/h, n ⫽ 3), moderate
(AHI, 15–30 events/h, n ⫽ 5), and severe (AHI ⭓ 30 events/h, n ⫽ 3)
sleep apnea (Table 1), with a comparable mix of sex and body mass
index. Seven patients were receiving CPAP, four of whom (subjects 3,
6, 9, and 10) participated in the study because they had difficulties
tolerating CPAP, with compliance defined as CPAP use for 4 hours or
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TABLE 1. ANTHROPOMETRICS AND SLEEP-DISORDERED BREATHING INDICES
Disease Severity
Mild
Moderate
Severe
Subject 1 Subject 2 Subject 3 Subject 4 Subject 5 Subject 6 Subject 7 Subject 8 Subject 9 Subject 10 Subject 11 Mean SEM
Anthropometric data
Sex
Age, yr
Height, cm
Weight, kg
BMI, kg/m2
Sleep-disordered breathing
AHI, events/h
HI, events/h
AI, events/h
Average base SaO2, %
Average low SaO2, %
M
33
168
70.9
25.2
M
24
190.5
120.9
33.2
M
49
180.0
74
22.6
F
39
152.4
63.9
27.4
F
31
160
70.9
27.6
M
56
182.9
91.7
27.4
F
42
154.9
169.1
70.3
M
53
172.7
72.0
24
F
70
157.5
60.0
24.1
M
77
182.9
86.8
25.9
F
56
172.7
66.67
22.35
5
4
1
96.7
94.5
8
7
1
95.2
93.4
13
12
1
94.2
92.3
19
19
0
97.5
93.3
20
20
0
96.5
92.4
21
20
1
96
91.3
22
19
3
97.3
91.9
30
26
4
94.7
90.9
39
4
35
97.2
87.1
46
29
17
93.8
87.3
58
23
35
95.4
90.4
49.7 5.0
170.7 4.1
81.9 12.7
30.5 4.3
27.7
17.9
9.8
95.8
91.0
4.7
2.4
4.3
0.4
0.7
Definition of abbreviations: AHI ⫽ apnea–hypopnea index; AI ⫽ apnea index; BMI ⫽ body mass index; HI ⫽ hypopnea index; SaO2 ⫽ oxygen saturation.
more per night, for 70% or more of nights. Patients were excluded if
they had central sleep apnea or serious medical conditions. Informed
consent was obtained from all subjects, and the Johns Hopkins University Institutional Review Board approved the protocol.
Study Procedures
Polysomnography. Polysomnography was performed with Somnologica
biosignal recording and analysis software (Embla, Broomfield, CO).
Signals included electroencephalograms (C3-A2, A2-O1), left and right
electrooculograms, submental electromyogram, tibial electromyogram,
electrocardiogram, oxyhemoglobin saturation, body position via infrared video camera, nasal cannula for measuring airflow (Nights 2 and
3), and thoracic and abdominal belts for measuring respiratory effort.
On Night 1, a pneumotachometer (21) attached to a nasal CPAP mask
(Respironics, Murraysville, PA) and a fluid-filled catheter (CooperSurgical, Trumbull, CT) were used to measure ventilation and supraglottic
pressure on and off TNI.
Nasal insufflation. An air compressor (Seleon, Freiburg, Germany)
delivered at the nose a constant flow rate of up to 20 L/minute, which
was the upper limit of the current technology, given the dimensions of
the cannula. A heater and humidifier regulated the temperature and
humidity. A heated wire was incorporated into the lumen of the nasal
cannula tubing to achieve a temperature of 30 to 33⬚C and relative
humidity of approximately 80% at the nasal outlet (Figure 1). (For
nasal cannula dimensions, see the caption to Figure 1).
sleep or oxyhemoglobin desaturation equal to or greater than 3%. Each
respiratory event (apnea and hypopnea) was subclassified as either
central or obstructive on the basis of assessment of the respiratory flow
and effort signals (supraglottic pressure catheter or abdominal and
thoracic plethysmography) (24). Body position was carefully monitored
during both the baseline and treatment nights, and an AHI for each
individual was calculated for the supine and side positions separately.
An overall AHI was then produced by weighting the time spent in each
body position on the first night. On the second night, we applied a
positional weighting factor from the first night to calculate an overall
AHI.
Arousal analysis. Arousals were scored as an abrupt shift in frequency that included ␪, ␣, and ␤ frequencies greater than or exceeding
16 Hz, but not spindles after a minimum of 10 consecutive seconds of
stable sleep, and arousals in REM were scored only if accompanied by
an increase in submental electromyogram amplitude (23). Assessment
Study Protocols
On Night 1 (titration night), subjects initiated sleep on 5 L/minute on
TNI for reasons of comfort. When subjects had established a stable
period (⬎ 10 min) of non–rapid eye movement (NREM) sleep, TNI
was applied at 0, 10, or 20 L/minute for 5-minute intervals in random
order. These trials were repeated a minimum of three times at each
TNI level in the supine position during NREM sleep.
Subjects were then randomized to separate nights on and off TNI
at 20 L/minute. Standard polysomnographic recording techniques were
employed to characterize sleep and breathing patterns on these nights.
On the basis of the findings in the TNI titration study, we anticipated
that patients who had predominantly hypopneas would experience a
greater effect than those who also had obstructive apneas.
Analysis
Polysomnography. Standard polysomnographic scoring techniques were
used to stage sleep (22), arousals (23), and respiratory events, which
were scored according to the “Chicago criteria” (24).
Respiratory indices. In brief, an apnea was defined as complete cessation of airflow for more than 10 seconds. Hypopnea was defined as
a greater than 30% reduction of airflow. Flow-limited events were
scored as hypopneas if airflow was reduced less than 30% compared
with adjacent breaths and was associated with either an arousal from
Figure 1. Nasal cannula for delivery of warm humidified air to a patient
(treatment with nasal insufflation). As can be seen, the cannula is designed to leave the nose open, and thus a patient can expire freely
through the nose. Dimensions of the cannula are as follows: length,
1,800 mm; outer diameter, 5 mm. Dimensions of the tube after the Y
piece: length, 440 mm each; inner diameter, 3.4 mm; dimension of
the prongs, 5 mm (outer diameter, each nostril). The cannula has been
designed to decrease any potential noise caused by the high flow of
air, minimizing noise-induced sleep disruption.
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of interrater variability was performed by two board-certified sleep
physicians in a subset of subjects (n ⫽ 9).
Breathing dynamics. End-expiratory pharyngeal pressure, peak inspiratory airflow, and respiratory effort were measured on the basis of
the 10 breaths immediately preceding and the last 10 breaths of each
TNI trial.
Statistical Analysis
Data are reported as means ⫾ SEM. A sign rank test was performed
(Stata 8; StataCorp, College Station, TX) to compare (1 ) differences
in polysomnographic indices between baseline diagnostic and clinical
treatment night and (2 ) differences in breathing dynamics on and off
TNI. p Values less than 0.05 were considered significant.
RESULTS
Subject Demographics
Eleven subjects (6 men and 5 women; age, 49.7 ⫾ 5.0 yr; body
mass index, 30.5 ⫾ 4.3 kg/m2) completed the study. By design,
our study population encompassed a wide spectrum from mild to
severe disease severity (Table 1). In general, patients with milder
disease severity had predominantly obstructive hypopneas (AHI,
5–15 events/h), whereas those with more severe sleep apnea (AHI,
⭓ 30 events/h) had many more obstructive apneas.
TNI Titration at 10 versus 20 L/Minute: Night 1
Figure 2 illustrates the effect of TNI at 10 and 20 L/minute on
air flow dynamics and supraglottic pressure in one subject with
predominantly obstructive hypopnea (subject 1, indicated by
open circles in Figure 4). Breaths off TNI (Figure 2, left) during
a hypopnea were characterized by a plateauing of inspiratory
flow as supraglottic pressure continued to fall, and snoring (microphone signal). A TNI flow rate of 10 L/minute (Figure 2,
middle) slightly increased end-expiratory supraglottic pressure
and decreased inspiratory effort swings. Nevertheless, inspiratory flow limitation and snoring persisted. In contrast, breaths
on TNI at 20 L/minute (Figure 2, right) were no longer flow
limited as indicated by a rounded inspiratory flow contour, an
increase in peak inspiratory airflow, a marked decline in supraglottic pressure swings, and the absence of snoring. Similar results were found in all our study participants.
Effect on Sleep-disordered Breathing Indices
In Figure 3, the effect of TNI at 20 L/minute on the sleepdisordered breathing pattern is illustrated for one subject with
obstructive hypopneas. Figure 3 (left) depicts two obstructive
hypopneas (see horizontal bars) as indicated by decreased inspiratory airflow, progressively increasing respiratory effort (Psg),
snoring (see microphone trace), and oxygen desaturations. When
TNI was administered (Figure 3, right), sleep and breathing
patterns stabilized, as reflected by the reduction in supraglottic
pressure swings, and resolution of inspiratory flow limitation,
snoring, and oxyhemoglobin desaturation.
In Figure 4, the sleep-disordered breathing responses of subjects to TNI (20 L/min) are presented for the clinical treatment
night (TNI on) and the baseline diagnostic night (TNI off). Two
main effects can be discerned. First, TNI led to a reduction in
the overall AHI (28 ⫾ 5 to 10 ⫾ 3 events/h, p ⬍ 0.01; Figure
4, left) and some improvement of the AHI was observed in each
subject (Figure 4, left). In eight of these subjects, the AHI fell
below 10 events/hour. Of the three remaining subjects, the nasal
cannula dislodged for 2.5 hours in one subject (Figure 4, left,
solid diamonds), and hence the AHI fell only minimally from
19 to 17, whereas more marked reductions in the AHI, from 46
to 27 and from 39 to 23 events/hour, were observed for the other
two (Figure 4, left, bars and plus symbols).
Second, TNI responses in hypopneas and apneas are shown
separately (Figure 4, middle and right, respectively). TNI decreased the hypopnea index (Figure 4, middle) from 18 ⫾ 2 to
8 ⫾ 2 events/hour (p ⬍ 0.01), and also reduced the number of
obstructive apneas in the three subjects who had an apnea index
greater than 10 events/hour during sleep (subjects 9, 10, and 11 in
Table 1, and represented by plus, bar, and solid triangle symbols,
respectively, in Figure 4, right). As can be seen, apneic subjects
9, 10, and 11 had a reduction in apnea index from 36 to 17, from
17 to 11, and from 35 to 6 events per hour of sleep, respectively,
suggesting that TNI can decrease apneas as well as hypopneas.
Assessment of interrater variability was performed with an intraclass correlation coefficient (ICC) for obstructive respiratory
events (ICC, 1.0), respiratory arousals (ICC, 0.98), and spontaneous arousals (ICC, 0.8), indicating good agreement between reviewers in all categories; disagreements between reviewers were
minor (Table 2).
Figure 2. Airflow and
supraglottic
pressure
(Psg) response to treatment with nasal insufflation (TNI) in one subject (subject 1). During
baseline, with TNI off
(left), large swings in supraglottic pressure and
flattening of the inspiratory airflow contour
occurred as supraglottic
pressure continued to
fall, indicating upper airway obstruction (left).
Whereas TNI at 10 L/
minute had no significant effect on airflow
and supraglottic pressure
swings (middle), TNI at 20 L/minute increased end-expiratory Psg from 0 to 2.2 cm H2O, which was associated with an increase in peak inspiratory
airflow from 290 to 360 ml/second, and respiratory effort markedly declined as indicated by reductions of the supraglottic pressure swings from
–15 to –3 cm H2O.
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197
Figure 3. Effect of treatment with nasal insufflation (TNI) on obstructive hypopneas in one subject during non–rapid eye movement (NREM) sleep.
Left: TNI off. Right: TNI 20 L/minute. Horizontal lines below the flow signal demarcate individual hypopnea events with oxyhemoglobin desaturations
of 4 and 3%, respectively. Note the marked decline in the snoring signal on TNI compared with TNI off. Microphone ⫽ digitally displayed snoring
auditory signal; Psg ⫽ supraglottic catheter pressure (cm H2O); SaO2 ⫽ oxygen saturation.
Mechanism of Action
To explore the underlying mechanisms responsible for the effect
of TNI on sleep-disordered breathing we assessed inspiratory
airflow, end-expiratory supraglottic pressure, and respiratory effort in a subgroup of subjects (n ⫽ 7). In Figure 5, the immediate
respiratory responses to TNI at a rate of 20 L/minute for one
subject with obstructive hypopneas are demonstrated. As can
be seen in Figure 5, breaths off TNI were characterized by
inspiratory flow limitation indicated by a plateauing of inspiratory flow as supraglottic pressure continued to fall (see inspiratory flow limitation threshold marked by the horizontal dashed
line). After TNI was initiated, there was an instantaneous increase
Figure 4. Sleep-disordered
breathing indices. Shown
are apnea and hypopnea indices during the
baseline (Bsl) diagnostic
night and the clinical
treatment night for individual subjects. Individual subject symbols
are consistent between
panels. TNI ⫽ treatment
with nasal insufflation.
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TABLE 2. INTERRATER RELIABILITY
Respiratory
Arousal Indices
AHI
Subject
Spontaneous
Arousal Indices
Scorer 1
Scorer 2
Scorer 1
Scorer 2
Scorer 1
Scorer 2
C
D
E
F
G
H
I
J
K
20
16
7
7
24
8
10
5
86
21
15
6
7
25
8
10
5
86
21
16
9
3
20
8
5
5
64
23
15
7
3
24
8
15
5
64
7
7
4
0
8
2
1
6
0
5
5
3
0
4
1
0
3
0
Mean
SE
ICC
20
26
20
26
1.00
17
19
18
19
0.98
4
3
2
2
0.80
Definition of abbreviations: AHI ⫽ apnea–hypopnea index; ICC ⫽ intraclass
correlation coefficient.
Individual data are presented for a subset of patients (n ⫽ 9), scored by two
experienced board-certified sleep medicine physicians, for the analysis of interscorer agreement for the apnea–hypopnea indices, respiratory and spontaneous arousal indices.
in end-expiratory supraglottic pressure (Figure 5, circled 1) and
mean inspiratory airflow (Figure 5, circled 2). Nevertheless, inspiratory flow limitation was still present over a short period of
breaths in which supraglottic pressure swings declined gradually
on a breath-by-breath basis (Figure 5, circled 3), indicating that
improvements in airflow were associated with progressive reductions in respiratory drive. Once the supraglottic pressure swings
no longer fell below the threshold for flow limitation (Figure
5, circled 4), the inspiratory airflow contour assumed a round,
non–flow-limited pattern (Figure 5, circled 5).
Pooled data for a subset of subjects (n ⫽ 7) demonstrate
that TNI increased end-expiratory pharyngeal pressure from
atmospheric to 1.8 ⫾ 0.1 cm H2O (p ⫽ 0.04), increased inspiratory
airflow from 255.1 ⫾ 54.2 to 363.5 ⫾ 26.7 ml/second (p ⫽ 0.04),
and decreased supraglottic pressure swings from 11.3 ⫾ 0.5 to
4.4 ⫾ 0.6 cm H2O (p ⫽ 0.04). Thus, TNI alleviates upper airway
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2007
obstruction through an immediate increase in pharyngeal pressure in combination with gradual reflexive reductions in ventilatory drive.
Sleep Characteristics and Arousal Indices
As shown in Table 3, TNI reduced the respiratory-related arousal
frequency (18 ⫾ 4 to 8 ⫾ 2 events/h, p ⬍ 0.01), without a change
in the spontaneous arousal frequency (3 ⫾ 1 to 3 ⫾ 1, p ⫽ 0.65).
There was no overall change in total sleep time, sleep efficiency,
or sleep stage distribution, perhaps as a result of our relatively
small sample size. However, each patient exhibited an improvement in sleep stage distribution, with either a greater percentage
of time in deeper stages of NREM sleep (subjects 3, 4, 5, 6, 8,
and 11) or a greater percentage of total sleep time spent in REM
sleep (subjects 1, 2, 7, 9, and 10), suggesting that TNI improved
sleep quality.
DISCUSSION
Our study was designed to examine the effect of treatment with
nasal insufflation (TNI) on obstructive sleep apnea. In a broad
spectrum of patients, we found a significant reduction in inspiratory flow limitation severity on TNI at 20 versus 10 L/minute, and
improvement in sleep apnea severity as reflected by a marked fall
in both the apnea–hypopnea and arousal indices on TNI at 20
L/minute. The relief of upper airway obstruction was most likely
due to small but consistent increases in pharyngeal pressure on
TNI, which decreased the severity of inspiratory flow limitation.
Mechanism of Action of TNI
To determine the mechanism of action of TNI, we assessed
airflow dynamics and supraglottic pressure responses to TNI at
a low rate (10 L/min) and a high rate (20 L/min) during periods
of hypopneas during NREM sleep. Whereas TNI at 10 L/minute
had no effect on airflow dynamics, TNI at 20 L/minute increased
peak inspiratory airflow and reduced supraglottic pressure
swings. Although these changes were relatively modest, sleep
and breathing patterns improved markedly in all subjects receiving TNI. These improvements can be attributed primarily to the
increase in pharyngeal pressure while receiving TNI. Inspiratory
airflow increases approximately 50 ml/second per cm H2O of
Figure 5. Mechanism of action. Airflow and supraglottic
pressure are shown during the
transition from flow-limited
breathing with TNI off, to non–
flow-limited breathing with
TNI at 20 L/minute. Psg ⫽
supraglottic catheter pressure
(cm H2O). Numbers in circles:
1, increase in end-expiratory
Psg; 2, increase in mean inspiratory airflow; 3, decrease in
supraglottic pressure swings
on a breath-by-breath basis; 4,
Psg threshold for inspiratory
flow limitation; and 5, a
round, non–flow-limited inspiratory pattern.
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TABLE 3. SLEEP CHARACTERISTICS AND AROUSAL INDICES
Baseline
TST, min
Sleep efficiency, %
NREM, % TST
Stage 1, %
Stage 2, %
Stage 1, %
REM, % TST
Arousal indices
Respiratory
Spontaneous
Total
TNI, 20 L/min
Mean
SEM
Mean
SEM
p Value
317.9
79.5
84.2
12.7
65.2
6.3
14.1
26.0
5.2
1.9
3.1
4.0
1.8
2.2
326.7
85.5
87.2
13.2
68.2
6.3
12.8
12.3
3.3
2.6
4.0
4.2
1.8
2.6
0.64
0.24
0.43
0.56
0.56
0.84
0.87
18.3
3.4
21.6
3.7
2.2
3.6
8.3
3.1
11.4
1.5
0.4
1.5
0.005
0.65
0.007
Definition of abbreviation: NREM ⫽ non–rapid eye movement; TST ⫽ total sleep
time.
Group data are presented for both the baseline and clinical treatment night
with TNI at 20 L/minute.
CPAP pressure applied (25). TNI at a rate of 20 L/minute led
to a similar increase in inspiratory airflow (45 ml/s per cm H2O).
The peak inspiratory airflows of our patients during hypopneas
were only mildly reduced to approximately 230 ml/second, and
rose to approximately 300 ml/second, a level previously associated with the elimination of inspiratory flow limitation and stabilization of breathing patterns (25). Thus, improvements in peak
inspiratory airflow were likely due to increases in pharyngeal
pressure, which were of sufficient magnitude to treat hypopneas
when inspiratory airflow levels are only mildly reduced.
Effect of TNI on Sleep-disordered Breathing
Although we expected marked improvements in the AHI primarily in patients with hypopneas rather than obstructive apneas,
TNI lowered the AHI in all subjects, regardless of the apnea–
hypopnea distribution. Although the primary mechanism of action appears to be related to increases in end-expiratory pharyngeal pressure, other factors may have further improved
ventilation in addition to alleviating upper airway obstruction.
First, even small increases in pharyngeal pressure may have
increased lung volume. Increases in lung volume lead to improvements in both oxygen stores and upper airway patency (26–30),
both of which may further stabilize breathing patterns during
sleep. As ventilation improved in our patients during sleep, enhanced sleep continuity (decreased arousal frequency) may have
also contributed to further reductions in the apnea–hypopnea
indices (31, 32). Indeed, we found a trend toward improvement
in sleep stage distribution in all subjects, with a reduction in
respiratory arousals, and no change in spontaneous arousals.
Additional benefits may have accrued from insufflating air directly into the nose, which may produce concomitant reductions
in dead space ventilation. Therefore, improvements in oxygen
stores, ventilation, and sleep continuity, along with enhanced
upper airway patency, are likely responsible for the beneficial
responses to TNI. We acknowledge that obstructive sleep apnea
was not completely eliminated in all of our patients, and that
nasal CPAP might still be more efficacious in reducing the AHI
during treatment nights. Nevertheless, reduced compliance with
CPAP can significantly compromise long-term therapeutic effectiveness, leaving a significant portion of patients untreated over
time (33). Poor CPAP compliance has been attributed to cumbersome masks, and to difficulties in exhaling against a high
backpressure (17). In contrast, TNI offers a simplified nasal
interface for delivering relatively low levels of pharyngeal pressure, which may enhance long-term compliance, and overall
199
therapeutic effectiveness, and thus might reduce long-term cardiovascular and metabolic complications of obstructive sleep
apnea.
Limitations
There are several limitations in the current study. First, we used
only flow rates of 10 and 20 L/minute in our study. It is possible
that higher flow rates would have been even more effective in
eliminating all respiratory events. However, we used relatively
low flow rates to balance the comfort of nasal insufflation with
efficacy. Indeed, there were no reports of significant discomfort
or side effects after a full night of treatment with TNI at 20 L/
minute, with the exception of reports that air temperatures were
either too warm (n ⫽ 2) or cold (n ⫽ 1) for initiating sleep.
Nevertheless, the majority of subjects did not have difficulty
initiating or maintaining sleep as compared with baseline. None
of the patients complained about noise related to the use of TNI,
which we acknowledge might result from patient motivation, or
perception relative to their previous experience with CPAP.
Moreover, assessment of sleep architecture between nights on
and off TNI indicates a trend toward improvement, without
change in spontaneous arousal indices. Second, it is possible that
the cannula may have dislodged during the night, accounting
for the treatment failure in at least one patient. Although it is
not yet clear how a minor dislodgement of the cannula can
affect efficacy, the fact that the majority of our patients had a
substantial reduction in sleep-disordered breathing indices suggests that the exact position of the nasal cannula is not critical.
Third, the occurrence of apneas might be dependent on body
position. We accounted for body position between the two
nights, thus eliminating the impact of a change in position on
the treatment effect. Fourth, TNI was used for only one night.
Although patients did not report any discomfort when using it
for one night, the response might be different when using TNI
repeatedly over several nights. Further studies of TNI administered over several nights would be required to examine its effect
relative to CPAP. Fifth, assessment of both spontaneous and
respiratory arousals is potentially associated with poor agreement between scorers. All data in this study were reviewed by
two experienced board-certified sleep physicians (H.S. and S.P.).
To assess quality assurance of our scoring, the interrater reliability was analyzed for a subset of patients (n ⫽ 9), and was comparable to previous assessments of interrater reliability of both spontaneous and respiratory arousal indices (ICC, 0.72; 95% confidence
interval: 0.44, 0.88) with experienced full-time scorers (34).
Implications
There are several clinical implications of our findings. First, our
findings provide evidence that TNI may offer a viable treatment
alternative to patients with obstructive hypopneas and apneas.
The finding that TNI alleviated obstructive hypopneas in all but
one patient predicts a high likelihood of treatment success in a
similar patient population. A retrospective analysis of our patient
database with 4,746 patients with obstructive sleep apnea–
hypopnea syndrome studied between 1981 and 2000, whose AHI
was greater than 10, showed that 28.4% of these patients had
predominantly obstructive hypopneas (more than 90% of all
events) and would meet the polysomnographic and anthropometric characteristics of our study population. Second, our findings that TNI also had an effect on obstructive apnea in our
patients with an apnea index of greater than 15 implies that TNI
may be beneficial in some patients with obstructive apneas as
well. Further studies are required to elucidate the polysomnographic and/or clinical predictors of a TNI response. Third, we
used a fixed flow rate and cannula size, which may obviate the
need for titration studies. Indeed, it may be possible to offer an
57
Therapie
Diagnose
TNI® Studien
200
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 176 2007
empiric, streamlined therapeutic approach with TNI for a large
proportion of patients with sleep apnea.
In summary, our study provides clinical proof of concept for
employing TNI as a novel treatment for patients with obstructive
sleep apnea–hypopnea syndrome. Because one flow rate and
cannula size was sufficient to stabilize breathing patterns in the
majority of our subjects, titration may be obviated, thereby
streamlining the initiation of treatment. Moreover, the minimally
intrusive nasal interface of TNI may improve patient adherence,
and may ultimately prove more effective in managing the longterm morbidity and mortality of sleep apnea. Further studies
will be required to extend these findings and to determine the
ultimate role of TNI in managing obstructive sleep apnea.
Conflict of Interest Statement : B.M.M. does not have a financial relationship with
a commercial entity that has an interest in the subject of this manuscript. S.P.P.
does not have a financial relationship with a commercial entity that has an interest
in the subject of this manuscript. J.P.K. does not have a financial relationship with
a commercial entity that has an interest in the subject of this manuscript. P.L.S.
does not have a financial relationship with a commercial entity that has an interest
in the subject of this manuscript. A.R.S. received $18,000 in 2006, under a private
licensing agreement between Dr. Schwartz and Seleon GmbH. The terms of this
arrangement are being managed by Johns Hopkins University in accordance with
its conflict of interest policies. H.S. received $78,000 from 2003 to 2006. Under
a private licensing agreement between Dr. Schneider and Seleon GmbH,
Dr. Schneider receives consulting fees (U.S. $18,000 in 2006) and is entitled to
royalty payments on the future sales of products described in this article. Under
a separate licensing agreement between Dr. Schneider and Seleon GmbH and
Johns Hopkins University, Dr. Schneider is entitled to a share of royalty received
by the university on sales of products described in this article. The terms of this
arrangement are being managed by Johns Hopkins University in accordance with
its conflict of interest policies. Funding for the study described in this article was
partially provided by Seleon GmbH.
Acknowledgment : The authors thank Mr. Peter DeRosa and Mr. Christopher
Smith for contributions to this study, which included technical support, data
collection, and help in the preparation of tables and figures.
References
1. Babu AR, Herdegen J, Fogelfeld L, Shott S, Mazzone T. Type 2 diabetes,
glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med 2005;165:447–452.
2. Punjabi NM, Shahar E, Redline S, Golttlieb DJ, Givelber R, Resnick HE.
Sleep-disordered breathing, glucose intolerance, and insulin resistance:
the Sleep Heart Health Study. Am J Epidemiol 2004;160:521–530.
3. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular
outcomes in men with obstructive sleep apnoea–hypopnoea with or
without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365:1046–1053.
4. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin
V. Obstructive sleep apnea as a risk factor for stroke and death. N
Engl J Med 2005;353:2034–2041.
5. Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive
sleep apnoea by continuous positive airway pressure applied through
the nares. Lancet 1981;1(8225):862–865.
6. Kushida CA, Morgenthaler TI, Littner MR, Alessi CA, Bailey D, Coleman
J Jr, Friedman L, Hirshkowitz M, Kapen S, Kramer M, et al.; American
Academy of Sleep. Practice parameters for the treatment of snoring
and obstructive sleep apnea with oral appliances. American Sleep
Disorders Association. Sleep 2005;18:511–513.
7. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep 1996;19:156–177.
8. Kribbs NB, Pack AI, Kline LR, Smith PL, Schwartz AR, Schubert NM,
Redline S, Henry JN, Getsy JE, Dinges DF. Objective measurement
of patterns of nasal CPAP use by patients with obstructive sleep apnea.
Am Rev Respir Dis 1993;147:887–895.
9. McArdle N, Deveruex G, Heidarnejad H, Engleman HM, Mackay TW,
Douglas NJ. Long-term use of CPAP Therapy for sleep apnea/hypopnea
syndrome. Am Rev Respir Dis 1999;159:1108–1114.
10. Eastwood PR, Szollosi I, Platt PR, Hillman DR. Comparison of upper
airway collapse during general anesthesia and sleep. Lancet 2007;359:
1207–1209.
58
11. Mansour KF, Rowley JA, Meshenish AA, Shkoukani MA, Badr MS. A
mathematical model to detect inspiratory flow limitation during sleep.
J Appl Physiol 2002;93:1084–1092.
12. Schwartz AR, Smith PL, Wise RA, Bankman I, Permutt S. Effect of
positive nasal pressure on upper airway pressure–flow relationships.
J Appl Physiol 1989;66:1626–1634.
13. Gleadhill IC, Schwartz AR, Schubert N, Wise RA, Permutt S, Smith PL.
Upper airway collapsibility in snorers and in patients with obstructive
hypopnea and apnea. Am Rev Respir Dis 1991;143:1300–1303.
14. Smith PL, Wise RA, Gold AR, Schwartz AR, Permutt S. Upper airway
pressure–flow relationships in obstructive sleep apnea. J Appl Physiol
1988;64:789–795.
15. Aloia MS, Stanchina M, Arnedt T, Malhotra A, Millman R. Treatment
adherence and outcomes in flexible vs standard continuous positive
airway pressure therapy. Chest 2005;127:2085–2093.
16. Drake CL, Day R, Hudgel D, Stefadu Y, Parks M, Syron ML, Roth T.
Sleep during titration predicts continuous positive airway pressure
compliance. Sleep 2003;26:308–311.
17. Olson EJ, Moore WR, Morgenthaler TI, Gay PC, Staats BA. Obstructive
sleep apnea–hypopnea syndrome. Mayo Clin Proc 2003;78:1545–1552.
18. Weaver TE, Maislin G, Dinges DF, Younger J, Cantor C, McCloskey S,
Pack AI. Self-efficacy in sleep apnea; instrument development and
patient perceptions of obstructive sleep apnea risk, treatment benefit
and volition to use continuous positive airway pressure. Sleep 2004;26:
727–732.
19. McGinley BM, Patil SP, Kirkness JP, Schwartz AR, Smith PL, Schneider
H. Continuous nasal airflow (TNI) through a nasal cannula treats
obstructive sleep hypopnea [abstract]. Proc Am Thorac Soc 2006;3:
A869.
20. McGinley BM, DeRosa P, Schwartz AR, Kirkness JP, Patil SP, Smith PL,
Schneider H. A novel strategy for treating upper airway obstruction
(UAO) with transnasal insufflation [abstract]. Sleep 2005;28:A208.
21. Hager DN, Fuld M, Kaczka DW, Fessler HE, Brower RG, Simon BA.
Four methods of measuring tidal volume during high-frequency oscillatory ventilation. Crit Care Med 2006;34:751–757.
22. Rechtschaffen A, Kales A. A manual of standardized terminology, techniques and scoring systems for deep states of human subjects.
Bethesda, MD: National Institutes of Health; 1968. NIH Publication
No. 204.
23. Sleep Disorders Task Force of the American Sleep Disorders Association. EEG arousals: scoring rules and examples. Sleep 1992;15:174–184.
24. American Academy of Sleep Medicine Task Force. Sleep-related breathing disorders in adults: recommendations for syndrome definition and
measurement techniques in clinical research. Sleep 1999;22:667–689.
25. Patil SP, Punjabi NM, Schneider H, O’Donnell CP, Smith PL, Schwartz
AR. A simplified method for measuring critical pressures during sleep
in the clinical setting. Am J Respir Crit Care Med 2004;170:89–93.
26. Heinzer RC, Stanchina ML, Malhotra A, Jordan AS, Patel SR, Lo YL,
Wellman A, Schory K, Dover L, White DP. Effect of increased lung
volume on sleep disordered breathing in patients with sleep apnoea.
Thorax 2006;61:435–439.
27. Hoffstein V, Zamel N, Phillipson EA. Lung volume dependence of pharyngeal cross-sectional area in patients with obstructive sleep apnea.
Am Rev Respir Dis 1984;130:175–178.
28. Series F, Cormier Y, Desmeules M. Influence of passive changes of lung
volume on upper airways. J Appl Physiol 1990;98:2159–2164.
29. Series F, Cormier Y, Lampron N, La Forge J. Increasing the functional
residual capacity may reverse obstructive sleep apnea. Sleep 1988;11:
349–353.
30. Stanchina M, Malhotra A, Fogel R, Trinder J, Edwards J, Schory K,
White DP. The influence of lung volume on pharyngeal mechanics,
collapsibility, and genioglossus muscle activation during sleep. Sleep
2003;26:851–856.
31. Wellman A, Malhotra A, Fogel R, Edwards JK, Schory K, White DP.
Respiratory system loop gain in normal men and women measured
with proportional-assist ventilation. J Appl Physiol 2002;94:205–212.
32. Younes M. Role of arousals in the pathogenesis of obstructive sleep
apnea. Am J Respir Crit Care Med 2004;169:623–633.
33. Grote L, Hedner J, Grunstein R, Kraiczi H. Therapy with nCPAP: incomplete elimination of sleep related breathing disorder. Eur Respir J
2006;16:921–927.
34. Whitney CW, Gottlieb DJ, Redline S, Norman RG, Dodge RR, Shahar
E, Surovec S, Nieto FJ. Reliability of scoring respiratory disturbance
indices and sleep staging. Sleep 2007;21:749–757.
Therapie
TNI® Studien
Diagnose
59
Therapie
Diagnose
Fallbeispiele
Erwachsene
TNI®20
Geschlecht: männlich
Diagnose:
Alter: 67 Jahre
Gewicht/Größe: 110 kg, 189 cm
COPD IV mit akuter Exazerbation (BODE 4), hochgradig respiratorische Globalinsuffizienz,
Chron. Cor pulmonale, mäßiggradiges zentrilobuläres Lungenemphysem
Bisherige Therapieform/Werte:
Sauerstofftherapie: 2l/min O2 in häuslicher Umgebung
pCO2: 64,6 mmHg
pO2: 39,9 mmHg
75,1%
sO2:
TNI®20 Therapie/Werte:
20l/min nur Raumluft (ohne Sauerstoffzugabe) Werte nach 12 Tagen
pCO2: 43,0 mmHg
pO2: 55,2 mmHg
sO2:
88,7%
Bewertung des Patienten: Wohlgefühl verbunden mit gutem Schlaf, Wunsch nach Therapiefortsetzung
Geschlecht: männlich
Diagnose:
Alter: 73 Jahre
Gewicht/Größe: 88 kg, 173 cm
Schwere OSA
Bisherige Therapieform/Werte:
TNI®20 Therapie/Werte:
CPAP
sO2: mindestens
RDI tot:
RDI–REM:
79 %
46,6
33,8
20l/min Raumluft
sO2: mindestens
RDI tot:
RDI–REM:
83 %
4
11,7
Bewertung des Patienten: guter Schlaf
Geschlecht: männlich
Diagnose:
60
Alter: 78 Jahre
COPD Stadium 4 mit respiratorischer Globalinsuffizienz
Bisherige Therapieform/Werte:
Sauerstofftherapie: 1l/min O2,
pCO2: 60 mmHg
pO2: 46 mmHg
sO2:
79%
TNI®20 Therapie/Werte:
20l/min Raumluft Werte nach: 30 min:
pCO2: 55mmHg
pO2: 56 mmHg
sO2:
88%
Therapie
Diagnose
Fallbeispiele
TNI®20 oxy / TNI®20s oxy
Geschlecht: männlich
Diagnose:
Alter: 50 Jahre
Gewicht/Größe: 145 kg, 170 cm
Obesitas-Hypoventilationssyndrom mit respiratorischer Globalinsuffizienz
Bisherige Therapieform/Werte:
Sauerstoff 3-4 l/min
Unter TNI®20s oxy:
Verbesserte Werte:
pCO2 Situation als Trend verbessert
Sauerstoffsituation unwesentlich verbessert
keine Sauerstoffzugabe
Nachtpersonal hat Therapie beendet, war nicht eingewiesen
Geschlecht: männlich
Alter: 78 Jahre
Diagnose:
COPD Stadium 4, hyperkapnisch, chronische Cor pulmonale mit respiratorischer Globalinsuffizienz, will nach eigener Aussage sterben, lehnt Maske ab
Ausgangswerte:
pCO2: ca 70 mmHg
sO2:
unter 45%
Bisherige Therapieform/Werte:
Sauerstofftherapie: 2l/min O2
pCO2: 75mmHg
sO2:
92%
TNI®20s oxy Therapie/Werte:
2l/min O2 und 12l/min Raumluft Werte nach 24 h Behandlungsdauer
pCO2: 50 mmHg
sO2:
92%
Bewertung des Patienten: bereits nach 2 h nachlassende Dyspnoe
Geschlecht: männlich
Diagnose:
Alter: 72 Jahre
Obesitas-Hypoventilationssyndrom
Bisherige Therapieform/Werte:
Sauerstofftherapie: 2l/min O2
sO2: 74%
TNI®20s oxy Therapie/Werte:
18l/min Raumluft Werte nach: 1h:
keine Verbesserung im Trend erkennbar
sO2: 74%
Sauerstofftherapie:
2l/min O2 und 18l/min Raumluft
Werte nach: 15 min:
pCO2: unverändert
sO2: 92%
Schlafnacht:
sO2: 74%
Bewertung des Patienten: Schläft so gut, wie lange nicht mehr
61
Therapie
Diagnose
Fallbeispiele
TNI®20 oxy / TNI®20s oxy
Geschlecht: weiblich
Diagnose:
Alter: 72 Jahre
AZ-Verschlechterung mit zunehmender Ruhe-Dyspnoe, vermehrte zentrale Bronchialzeichnung und deutliche zentrale und periphere Stauungszeichen sowie ein pneumonisches
Infiltrat mit freiem Erguss im rechten Unterlappen
Therapie
Ausgangssituation
ohne
Sauerstofftherapie
3l/min O2
TNI®-Therapie
TNI® 16+5 O2
TNI® 16+5 O2
TNI® 16+5 O2
Gegencheck
ohne
4l/min O2
Datum/Zeit
pCO2
pO2
sO2
11.07.07 / 12.32 h
29 mmHg
47 mmHg
87%
11.07.07 / 13.00 h
31 mmHg
54 mmHg
90%
11.07.07 / 14.55 h
11.07.07 / 16.11 h
12.07.07 / 8.03
30 mmHg
33 mmHg
33 mmHg
62 mmHg
65 mmHg
62 mmHg
94%
95%
93%
13.07.07 / 8.41 h
14.07.07 / 10.12 h
32 mmHg
35 mmHg
43 mmHg
62 mmHg
83%
93%
Bemerkung: Mit nur O2 konnten die Blutgase nicht aufrechterhalten werden, was unter TNI® nicht der
Fall war. Unter TNI®-Therapie: gute Oxygenierung, niedrigere CO2 Werte, daher die bessere
Alternative zur reinen O2 Gabe
Geschlecht: männlich
Diagnose:
Alter: 75 Jahre
COPD Stadium 4 mit respiratorischer Globalinsuffizienz, Pneumonie beidseitig, nach
Acetabul umfraktur zunehmende Dekompensation, Ruhe-Dyspnoe, somnolent
Bisherige Therapieform/Werte:
NIV Beatmung (BiPAP, p=18/10 mbar, AF: 15/min),
Patient hat Maske nicht toleriert
TNI®20s oxy Therapie/Werte:
8l/min O2 und 14l/min Raumluft
pCO2: 39 mmHg
pO2: 78 mmHg
sO2:
95,9%
Bemerkung: Stabilisierung der Blutwerte ohne NIV, Entlassung auf Normalstation
62
Therapie
Diagnose
Fallbeispiele
TNI®20 oxy / TNI®20s oxy
Geschlecht: weiblich
Diagnose:
COPD mit akuter Exazerbation
Aufnahme der Pat.
Stat. 1 wegen klin.
CO2 Narkose
Stat. 1
Stat. 2 Rückverlegung
Beginn High-Flow
Stat. 2
10 min vor Transport
auf D1 wegen Sepsis
Stat. 1 Transport
ohne High-Flow
Stat. 1
Therapie
2 lpm O2 über Brille
pO2 (mmHg)
71
pCO2 (mmHg)
54
4 lpm O2 über Brille
217
135
2 lpm O2 über Brille
20 lpm High-Flow
(4 lpm O2 /16 lpm Luft)
20 lpm High-Flow
(4 lpm O2 /16 lpm Luft)
20 lpm High-Flow
(4 lpm O2 /16 lpm Luft)
67
105
42
88
50
80
54
48
CPAP mit 6 lpm O2
44
77
Castor Helm 7 lpm O2
66
91
Bemerkung: Durch die Atmungsunterstützung kann die Erschöpfung der Atemmuskulatur kompensiert
werden, die mangels Kraft zu einer flachen Atmung mit verminderter Ventilation der Lunge
führt und keine suffiziente O2-Aufnahme ermöglicht. Durch den aufgebauten PEEP wird der
expiratorische Kollaps der Atemwege bei der COPD verringert und eine suffiziente CO2Abatmung erreicht. Die Patientin hat den hohen Fluss sehr gut akzeptiert.
Fallbeispiel
Flow / O2
Ohne CO2 / O2
16/2
8,4/6,8
18/2
8,5/5,3
20/2
8,3/6,8
30 min
1,5 h
2,5 h
4h
8,2/6,7
8,1/6,5
8,1/7,2
8,2/6,9
8,1/6,3
7,9/7,1
7,8/6,8
7,3/6,9
7,2/7,0
7,6/6,6
6h
7h
9h
7,6/6,9
7,5/7,6
7,8/6,5
7,7/6,9
7,6/6,7
7,9/6,8
63
Therapie
Diagnose
Fallbeispiele
TNI®20 oxy / TNI®20s oxy
Geschlecht: männlich
Diagnose:
Alter: 72 Jahre
1. Bronchial – CA re OL, T2 N2 Mx, inoperabel wegen
2. schwere COPD mit respiratorischer Globalinsuffizienz
Problem: schwere, insbesondere nächtliche Dyspnoe, häufiges nächtliches Alarmieren des
ärztlichen Notdienstes.
Ruhe – BGA:
O2:
52 mm Hg
CO2: 48 mm Hg
Weiterhin phasische nächtliche Entsättigungen bis
minimal 65 %
Ruhe – BGA unter 2,5l O2:
O2 :
59 mm Hg
CO2: 56 mm Hg, somit wegen CO2-Retention O2 – Gabe
über Nasensonde nicht möglich.
Bisherige Therapieform/Werte:
BIPAP-Therapie mit O2-Gabe bei subjektiver Unverträglichkeit und
deutlich überblähter Lunge gescheitert (FEV1: o,7 l; ITGV 180 % Soll,
TLC 160 % Soll)
TNI®20 oxy Therapie/Werte:
2l/min O2 und 16l/min Raumluft:
Ruhe – BGA: O2:
65 mm Hg
CO2: 43 mm Hg
Bemerkung: Subjektiv beschwerdefrei, nächtliches Durchschlafen möglich, nächtliche Mindestsättigung:
85 % (versus 65 % vor Therapie)
Geschlecht: männlich
Diagnose:
64
Alter: 72 Jahre
1. Zentrale schlafbezogene Atmungsstörung ( AHI 40 pro Stunde ) bei
2. Morbus Parkinson
3. Z. n. apoplektischem Insult
Bisherige Therapieform/Werte:
CPAP / BIPAP: Therapie wegen Maskenintoleranz nicht möglich,
O2: Insufflation per Nasensonde (2l und 4l) ohne Effekt auf AHI
TNI®20 oxy Therapie/Werte:
2l/min O2 und 18l/min Raumluft:
AHI 11 pro Stunde und deutliche Besserung der Tagessymptomatik.
Therapie
Diagnose
Fallbeispiele
Kinder
TNI®20
Fallbeispiel 1-jähriges Kind:
Erfolgreiche Atmungsunterstützung eines ehemals Frühgeborenen mit nasaler Insufflation
Zusammenfassung des Fallbeispiels: Der Patient war ein 1-jähriger Knabe, ehemaliges Frühgeborenes
der 27. SSW, mit multiplen Erkrankungen: akute respiratorische Insuffizienz, Epilepsie, infantile Zerebralparese, Tetraspastik, Retinopathie, BDP, Versorgung eines Gastrostromas und Bronchopneumonie. Er wurde mit
fieberhaftem, pulmonalem Infekt mit deutlich obstruktiver Komponente stationär in die Abteilung eingewiesen.
Durch reichliche tracheobronchiale Sekretion lag eine akute respiratorische Insuffizienz mit Hypoxämie und Hyperkapnie vor. Eine zunehmende Verschlechterung der pulmonalen Situation mit einer Sauerstoffentsättigung
zwischen 9% und 25% (über Monitor bestimmt) konnte trotz intensivem Absaugen von Sekret und der Gabe
von Sauerstoff nicht verhindert werden. Unter Sedierung wurde danach die nasale Insufflation mit initialem
Fluss von 10-12 Liter/min medizinischer Luft und zusätzlich 3-4 Liter/min Sauerstoff über 24 Stunden angewendet. Nach erfolgter Stabilisierung konnte der Fluss auf 8 Liter/min Luft und 1-2 Liter/min Sauerstoff reduziert
werden. Die Therapie wurde mehrere Tage bis zur deutlichen Besserung der pulmonalen Situation angewandt.
Fallbeispiel Frühchen (w): aus der 38. Schwangerschaftswoche
Diagnose:
Eutrophes Neugeborenes aus der 38.Schwangerschaftswoche
CHARGE-Syndrom, zentrales Schlafapnoe-Syndrom, rezidivierenden Apnoeanfällen,
z.n.Aspirationspneumonie
Bisherige Therapieform/Werte:
NIV Beatmung, hat Maske nicht toleriert
TNI®20 Therapie:
wird gut akzeptiert, durchschnittliche sO2 Abfälle
Fallbeispiel 3 jähriger (m)
Diagnose:
Schwerstes obstruktives Schlafapnoe-Syndrom
M.Crouzon mit multiplen Nahtsynostosen, betont im Bereich der Coronar- und Sagittalnähte,
z.N. Choanalstenose, operative Erweiterung bds. 06/06, Einsatz von intranasalen Platzhatern
Bisherige Therapieform/Werte:
NIV Beatmung, hat Maske nicht toleriert
TNI®20 Therapie:
wird gut akzeptiert
Fallbeispiel 3 jähriger (m)
Diagnose:
Schwerstes obstruktives Schlafapnoe-Syndrom
Freie Trisomie 21 mit typischen dysmorphen Stigmata, extreme psychomotorische Entwicklungsstörung, z.N. atrioventrikulärem Septumdefekt, AV-Klappen Insuffizienz, sekundärer
pulmonaler Hypertonie
Bisherige Therapieform/Werte:
NIV Beatmung, hat Maske nicht toleriert, autistisches Einschlafritual,
daher Maskenanpassung nicht möglich
TNI®20 Therapie:
wird gut akzeptiert, subjektiv und objektiv OSAS deutlich besser
65
Therapie
Diagnose
Über uns
Die TNI medical AG entwickelt, produziert und vertreibt Diagnose- und Therapiegeräte im
Bereich der Atmungsunterstützung. Unsere Therapieprodukte sind in erster Linie für die
Behandlung des Patienten zu Hause bestimmt, vor allem auch während des Schlafs. Mit
ihrer neu eingeführten TNI® Atmungsunterstützung fokussiert die TNI medical AG auf eine
Maximierung des Patientenkomforts bei gleichzeitiger Vereinfachung der Anwendung.
Das führt auch zu einer höheren Kosteneffizienz.
Das Unternehmen mit der Firmenzentrale in Freiburg und weiteren Sitzen in Würzburg
und Dessau wurde im Herbst 2007 als Spin-off der seleon gmbh gegründet, einem weltweit führenden Technologieunternehmen im Bereich der mechanischen Atmungstherapien. Die mit unseren Anwendungen primär behandelten Krankheitsbilder Schlafapnoe
und chronisch obstruktive Lungenerkrankung zeigen derzeit weltweit die höchsten Fallzuwachsraten.
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66
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Diagnose
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