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The management of severe The management of severe

The management of severe - PowerPoint Presentation

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The management of severe - PPT Presentation

hypoxaemic respiratory failure in critical care Simon Baudouin Senior Lecturer in Critical Care University of Newcastle Conventional definitions Type 1 PaO 2 lt 8 kPa on air Type 2 PaO 2 ID: 1047541

niv care amp critical care niv critical amp acute respiratory peep ventilation lung patients copd failure admissions conventional intubation

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1. The management of severe hypoxaemic respiratory failure in critical careSimon BaudouinSenior Lecturer in Critical CareUniversity of Newcastle

2. Conventional definitionsType 1 PaO2 < 8 kPa on airType 2 PaO2 < 8 kPa on air & PaCo2 > 6 kPaNot helpful!Ultimately all severely ill patients become hypercapnic without interventionAcuteChronicAcute on chronicReach ITU v intubate in EAURespiratory failure

3. Hypoxaemia – V/Q mismatch & shuntHypercapnia HypoventilationIncrease in deadspace ventilationV/Q mismatchRespiratory Failure - pathophysiology

4. The magnitude of COPD in the UKUk National COPD audit 2003; Thorax 2006;61:837-842234 UK acute hospitals40 consecutive acute COPD admissions7259 patients90 day readmission rate 31.4%!

5. The magnitude of COPD in the UK16-47% hypercapniaHalf will need ventilatory support - Plant et al, Thorax, 2000; 55: 550-554 - 1 year survey in Leeds  983 admissions  2.2% ICU admissions  73% hospital mortality in ICU admissions70 NIV patients/year/250,000 population

6. Aetiology of Respiratory failureExplanation of hypoxaemia and hypercapniaMultiple inert gas elimination Broad V/Q distributionHypercapnia = ventilation to under-perfused unitsHypoxaemia = shuntingRespiratory muscle fatigue?Altered central drive?

7. Oxygen treatmentHypoxaemia is usually correctable with low flow O2The optimal target SaO2 is unknown > 90% - O2 dissociation curve > 85% (ARDS net)One small study (n = 36) 6.6hPa v 9.0 hPa - no difference (underpowered)High flow O2 will worsen HypercapniaChange to controlled O2 will reduce PaCO2

8.

9. NIV in acute exacerbations of COADpH < or = 7.35Mortality %

10. Randomised controlled trials in NIVEarly use of non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease on general respiratory wards: a multicentre, randomised, controlled trial.Plant et al. Lancet, 2000; 355: 1931-35 14 UK Hospitals n = 236 Mortality p = 0.05Intubation p = 0.02

11. Cochrane review &meta-analysis for COADBMJ 2003;326:185-190Typical UK hospital will avoid 3-9 ICU admissions/yearSave £12,000-53,000

12. NIV in A&E“The use of non-invasive positive pressure ventilation in the emergency department”RCT6/12 studyNIV vs. conventional support87 screened - 34 “immediate” intubation - 27 entered - 11 conventional - 16 NIVWood. Chest, 1998; 113: 1339-46

13. Time to intubation Standard 4.8 hrs NIV 26.0 hrsNIV in A&E

14. Critical Care for All? Should all patients receive NIV in a critical care area? No RCTs Majority of trials are in Critical Care areasPlant

15.

16. NIV in exacerbations of COADRecommendations of the COAD and NIV Standards of Care sub-committees of the British Thoracic Society, RCP & Modernisation AgencyEvery acute admissions unit should have an NIV service

17. Predicting outcome with NIV - Failure rate 7-50% - delay intubation  Acidosis  APACHE II - Indications for HDU admission  For intubation if NIV fails  Initial pH 7.25 or less  Worsening pH on NIV

18. Indications for intubationPatient choiceFailure of NIVUsually obvious clinicallyFatigued “awful looking” patientWorsening hypercapnia and LOCA&E arrest/peri-arrest situation

19. Longer-term issuesPatient/ventilator interactionsWeaningTracheostomyNutritionThe “unweanable” patient

20. WeaningRapid trial of extubation (onto NIV)Early tracheostomyRegular Sedation cessationWeaning protocolsA little progress every day!

21. Weaning with NIVN=43 (most with COADfailed wean for 3 daysShorter ICU & hospital LOSLess need for tracheostomy90 day survivalAm J Respir Crit Care Med 2003;168:70-6

22. Longer term outcome in COPD

23. SummaryCOPD admissions will increaseNIV is effective in both survival and prevention of intubationOutcome of ventilation in COPD is no worse than in other conditionsPatient choice and informed decisions

24. Previously fit 24 year old womenFirst pregnancyNo problems until week 35“Cough and cold”“Shivery”Increasingly breathless over 24 hoursBrought to maternity ward by husbandClearly very unwellSaO2 air 79%RR 35/minCrackles ++Foetus aliveCritical Care outreach calledThe new 21st century critical care

25. Treatment with steroids

26. Early corticosteroids in severe influenza A/H1N1 pneumonia and acute respiratory distress syndrome.Am J Respir Crit Care Med. 2011 May 1;183(9):1200-6.French national registry – no benefit; possible early harmCorticosteroids in severe H1N1pneumoniaEuropean SICM databaseCox analysis no benefit from steroids

27. Critical Care obstetric intensivistSeparate the two patientsFoetus is viableVentilation for the Mother is inevitableExperience from other unitsUrgent Caesarean sectionVentilated with Critical Care ventilator during sectionHealthy girl deliveredMother transferred to critical care unitDelivery?

28. Invasive Mechanical VentilationSubstitute for the respiratory muscle pumpComplex multi-functional machinesEfficacy established during polio epidemics 1960sLed to development of modern, centralised critical care services

29. Ventilator-induced lung injuryBroncho-pulmonary dysplasia Well + Tierney 1974 - rats ventilated with peak airway pressures 45 cm H2O developed pulmonary oedemaCarlton 1990 - Lung overexpansion increases lymph flow in lambsLymph flow ml/Kg

30. Ventilation with lower tidal volumes as compared with traditional volumes for acute lung injury and the acute respiratory distress syndromeMortality at 180 daysProtection 31.0%Conventional 39.8%P = 0.007

31. Lung compartments in ARDSNormal lungPartial collapse/floodingComplete collapserecruitable

32. Does PEEP recruit lung in ARDS?5 cm PEEP5 cm PEEP

33. Fluid management in ARDSN = 100060 day mortalityLiberal v conservative fluid

34. Fluid management in ARDSImproved oxygenationIncreased ventilator free daysNo increase in shock or dialysis

35. N = 549How much PEEP?Higher versus lower PEEP in patients with ARDSNew Engl J Med 2004;351:327-336Lower PEEP = 8 cm H2OHigher PEEP = 13 cm H2O

36. Often improves oxygenationProposed mechanisms - recruitment of dorsal collapsed lung units - improved respiratory mechanics - increased secretion drainage - decreased injury from mechanical forcesProne positioning in ARDS

37. Prone positioning in ARDSN=304N=791

38. Initial improvement in PaO2/SaO2 to 90%Gradual fall to SaO2 84%CXR – no mechanical cause07:00

39. Rescue = desperationRescue = no high grade evidenceRescue = risks as well as possible benefitsOscillator ventilationECMO“Rescue therapy in ARDS”

40. Rate 60 – 100 bpmTV below anatomic deadspaceAlveoalar derecruitment & overdistention limitedHigh frequency ventilation

41. Large, multi-centre RCTConventional v high frequency ventilationComplete recruitment 2012Over 800 patients

42. ECMO

43.

44. Outcome in 1 ECMO centre (Glenfields)Protocolised careExperienced expertsAverage outcome in92 conventional centres11 referral centresNon protocolised careVariable experienceVariable clinical cover/teamWhat is the Cesar trial comparing

45. Hypoxaemia is the greatest immediate threatSevere oxygen induced hypercapnia is rareOxygen induced hypercapnia only occurs in chronic respiratory failurePreviously well patients with hypercapnia are severely illHypercapnia does not equate to COPDRespiratory failure