Den hyperkapniska triangeln. Bengt Midgren Skånes Universitetssjukhus Lund

Transkript

1 Den hyperkapniska triangeln Bengt Midgren Skånes Universitetssjukhus Lund

2 Hyperkapnisk kronisk respiratorisk insufficiens OBESITAS OSA KOL

3 Kronisk hyperkapni vid KOL Uppträder sent i sjukdomens naturalförlopp Beror definitionsmässigt på en alveolär hypoventilation Men beror inte på egentlig hypoventilation = låg minutventilation!

4 West JB. Causes of carbon dioxide retention N Engl J Med 1971; 284:1232 Hypercapnia in COPD is not due to hypoventilation, but to the patient s inability to increase his ventilation to the extent that is necessary to maintain a normal alveolar ventilation (VA) in lungs with severe ventilation-perfusion mismatch

5 Minutventilation Alveolär ventilation Dead-spaceventilation Normal KOL utan CO2- stegring KOL med CO2- stegring

6 Ishockeykurvan klubban PCO 2 Upprätthålls till priset av stigande minutventilation 25-30% FEV 1

7 Svenska LTOT-patienter (Swedevox) 75 år FEV 1 37%pred BMI 24 (17% har BMI >30) PaO 2 6,5 (urvalskriterium) PaCO 2 6,2 kpa PaCO 2 starkt korrelerat till FEV 1 BMI men inte till ålder

8 Ishockeykurvan PCO 2 * Svenska 25-30% KOL-LTOT-patienter, BMI 24, ålder 75 år FEV 1

9 Ishockeykurvan PCO 2 * Svenska KOL- LTMV-patienter, BMI 28, ålder 69 år 25-30% FEV 1

10 Ishockeykurvan PCO 2 Tyska KOL- LTMV-patienter, BMI 28, ålder 63 år * 25-30% FEV 1

11 Hyperkapnisk kronisk respiratorisk insufficiens OBESITAS OSA KOL

12 Kronisk hyperkapni vid obesitas OHS definieras som hyperkapni i vakenhet vid BMI > 30 i frånvaro av andra orsaker till hypoventilation Populationsestimat 0,3 % (Amanda Piper) Ca 1000 svenskar behandlas med hemrespirator pga OHS = 0,01%

13 Kronisk hyperkapni vid obesitas 50% av hospitaliserade patienter med BMI > 50 Nowbar et al 2004 Men ingen specifik BMI- cut off när man måste ta arteriell blodgas.

14 Relationen BMI PaCO 2 PaCO 2 BMI

15 OHS - mekanismer Högre andningsarbete hos OHS-patienter jämfört med lika feta eukapniska Mer central fettfördelning hos OHS-patienter jämfört med lika feta eukapniska OSA hos 90% av OHS-patienter Dagsymptomen vid OHS samma som vid OSA

16 Dagsymptom vid LTMV

17 Epworth vid LTMV

18 Semin Respir Crit Care Med 2009; 30:

19 Clinical presentation of OHS Most, but not all, patients with OHS will have some daytime respiratory complaints and some degree of excessive daytime somnolence. All the other complaints seen in the more typical eucapnic patient with OSA may also be present, including fatigue, somnolence (which can be mild or severe), mood disturbance, impaired concentration and memory, sleep disruption with snoring and choking, and morning headaches.

20 Clinical presentation of OHS Evidence of right ventricular dysfunction is seen in some patients with OSA uncomplicated by hypercapnia Overt cor pulmonale is extremely uncommon in OSA in the absence of hypercapnia Most patients with OHS (hypercapnia) will eventually show signs of circulatory congestion and cor pulmonale.

21 Clinical presentation of OHS The typical presentation of patients with OHS falls into two main patterns that differ primarily in the route by which the patient comes to clinical attention. Patients either present as part of the general OSA population or after an episode of severe respiratory failure, often precipitating a stay in the intensive care unit (ICU). Published series of OHS have tended to show different findings depending on which of these groups predominated.

22 Andningsdrive vid OHS Sänkt, men ej genetiskt Reversibelt vid behandling Leptin smalhormonet Bildas i fettväv Sänker aptiten Stimulerar andningen Starkt positivt samband leptin PCO 2 Leptinresistens analogt med insulinresistens vid DM typ II

23 Hyperkapnisk kronisk respiratorisk insufficiens OBESITAS OSA KOL

24 Kronisk hyperkapni vid OSA Inte välstuderat 10-20% av populationen vid sömnklinik?? Äldre arbeten, selekterat material Mina erfarenheter i oselekterat material Synnerligen ovanligt Om PaCO 2 inte över 6,5 går det utmärkt att behandla med vanlig CPAP

25 Kronisk hyperkapni vid OSA Mekanismer? Repetitiv transient hyperkapni ger resetting av ph-receptorerna i medulla oblongata AHI korrelerar dåligt till PaCO 2 Durationen av apnéerna mer väsentlig än index?

26 AHI 70

27 AHI 40

28 Kronisk hyperkapni vid OSA Mekanismer? Repetitiv transient hyperkapni ger resetting av ph-receptorerna i medulla oblongata Aggraverande faktorer Obesitas Andningsdeprimerande substanser KOL

29 Semin Respir Crit Care Med 2009; 30: Något missvisande titel, handlar mest om hur OSA övergår i kronisk hypoventilation

30 How to identify the patient? The hypercapnic patient who presents [to the sleep lab] will frequently be unrecognized initially if blood gases are not drawn It is only on careful analysis of the sleep study that hypoventilation will be suspected from the prolonged, rather than intermittent, desaturation pattern seen during the night

31 How to identify the patient? Our practice is to obtain blood gases (specifically arterial PCO 2 ) in any patient presenting with a history suggesting OSA who also has either an elevated venous bicarbonate level and/or associated chronic obstructive pulmonary disease (COPD) or predisposition to respiratory depression (e.g. drugs).

32 Therapy A review of our laboratory s experience in patients with chronic daytime hypercapnia showed that 50% of hypercapnic patients with OSA required only CPAP, whereas the remainder were diagnosed with SHVS and required therapy with noninvasive bilevel ventilation in addition to CPAP. It is rarely necessary to provide supplemental O 2 to keep the O 2 saturation above 90%.

33 Patofysiologi Effects of periodic breathing on acute CO 2 loading Magnitude of compensation for CO 2 accumulated during apnea/hypopnea This is ultimately limited by the 1) duration available and 2) magnitude of ventilation during the compensatory phase between apneas

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35 Interaktion med opiater impaired CO 2 homeostasis after respiratory events (e.g., the relative shortening of the interapnea duration and the reduced postevent ventilation) may be mediated by opioids or opioid receptors because endorphin blockade changed this pattern. These observations provide a framework for understanding the facilitating effect that opiates (including methadone) may have on the development of hypercapnia in some patients with OSA.

36 Mekanism 1 Immediate ventilatory compensation is required after each acute hypercapnic insult (apnea/hypopnea or sustained periods of hypoventilation). Ventilatory compensation may be compromised by either reduced ventilatory drive (e.g. reduction in ventilatory drive or induced by drug or oxygen) or reduced ventilatory efficiency of CO 2 clearance (e.g. as in underlying lung disease or congestive heart failure).

37 Mekanism 2 Adequate renal bicarbonate excretion is required during wakefulness to offset the effects of uncompensated cyclical hypercapnia. Renal compensatory mechanism may be compromised by diuretic induced chloride deficiency and/or by increased sodium avidity (e.g., CHF, hypoxia, or metabolic syndrome) and contribute to the transition between acute hypercapnia and the chronic hypercapnic state.

38 Hyperkapnisk kronisk respiratorisk insufficiens OBESITAS OSA KOL

39 Så här tror Bengt att verkligheten ser ut Obesitas OSA G473 OHS E662

40 Hyperkapnisk kronisk respiratorisk insufficiens OBESITAS OSA KOL

41 Overlap syndrome the overlap syndrome, in which obstructive sleep apnea is combined with chronic obstructive lung disease in the same patient DC Flenley 1985 Clin Chest Med

42 Overlap syndrome Prevalence and clinical feature of the "overlap syndrome", obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD), in OSA population. Rizzi et al 1997 Sleep Breath

43 Rizzi et al. In conclusion, an associated COPD is observed in more than 19% of OSA patients. Overlap patients are at increased risk of developing pulmonary hypertension and show a poorer quality of sleep as compared with OSA patients. The possibility of developing cor pulmonale should be given particular attention in the diagnosis and follow-up of Overlap patients.

44 Concomitant COPD and OSA. Hypercapnia not inclusion criterion

45 18,9% 18,5%

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49 Overlap syndrome COPD + OSA (1985) COPD + asthma (2009)

50 The overlap syndrome of asthma and COPD: what are its features and how important is it? Gibson PG, Simpson JL Thorax 2009

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52 Hyperkapnisk kronisk respiratorisk insufficiens OBESITAS OSA KOL

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54 PCO2 Alveolära gasekvationen PO 2 + 1,25*PCO 2 = 2017 Pensionärsrabatt PO2

55 Case #1 Smoking male, 70 years old Regular visit to the COPD outpatient office VC 2,9 (4,4) FEV 1 1,2 (2,8) FEV% 40 PO 2 7,3 PCO 2 6,5 BE +7

56 Case #1 Now calling for an extra visit because of swollen legs Unchanged blood gases Seen by a not-copd-doctor (me) Questions COPD as the single cause of hypercapnia BMI 36

57 Case #1 Regular visit to the COPD outpatient office VC 2,9 (4,4) FEV 1 1,2 (2,8) FEV% 40 PO 2 7,3 PCO 2 6,5 BE +7 BMI 36

58 Normala relationen mellan FEV 1 och PCO 2 vid KOL PCO 2 * 25-30% FEV 1

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60 PCO2 Blodgas före behandlingsstart 15 7,3 + 1,25*6,5 = 15, PO2

61 PCO2 Blodgas efter en tids behandling 15 8,2 + 1,25*5,4 = 14, PO2

62 PCO2 Blodgas efter ytterligare ett år 15 10,8 + 1,25*5,0 = 17, PO2

63 Alveolära gasekvationen PCO2 1. Ren hypoventilation 2. Lungfibros 3. Vanlig KOL 5, Hypoventilation med sekundär lungpåverkan 2 PO2 8 13

64 Hyperkapnisk kronisk respiratorisk insufficiens OBESITAS OSA KOL

65 All that wheezes is not asthma But it may not be COPD either. Hur skall vi handlägga en fet person med KOL och högt PaCO 2?

66 LTMV i Sverige

67 Komorbiditet enl Swedevox Lungsjuka: 20% bidiagnos OHS OHS: 24% bidiagnos lungsjukdom

68 LTMV lungsjukas fysiologi

69 63 år, BMI 28 Olika fenotyper som får/behöver LTOT och LTMV?

70 Ishockeykurvan PCO 2 * Svenska 25-30% KOL-LTOT-patienter, BMI 24, ålder 75 år FEV 1

71 Ishockeykurvan PCO 2 * Svenska KOL- LTMV-patienter, BMI 28, ålder 69 år 25-30% FEV 1

72 Ishockeykurvan PCO 2 Tyska KOL- LTMV-patienter, BMI 28, ålder 63 år * 25-30% FEV 1

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75 Sonstige Besonderheiten Die Einleitung einer NIV bei fortgeschrittener COPD fordert ein hohes Maß an Motivation und Mitarbeit von Seiten des Patienten und ist für das therapeutische Team eine besondere Herausforderung. Deshalb kann die stationäre Behandlungszeit bis zum Erreichen einer stabilen Therapie eine bis zwei Wochen in Anspruch nehmen [Windisch et al, 2002c] [Windisch, 2008] [Sivasothy et al, 1998]. Bei den oft älteren, multimorbiden Patienten ist dieser Zeitaufwand gerechtfertigt, um eine optimale Anpassung von Beatmungsmodus und Maske an die Bedürfnisse des Patienten zu er-zielen und um die langfristige Adhärenz des Patienten zu gewährleisten [Criner et al, 1999].

76 Hyperkapniska triangeln OBESITAS OSA KOL

77 Multipel börda och litet glädje? 100 kg