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Respiratory Failure and Mechanical Ventilation Management, dr Dafsah
- 1. Managment of Acute RespiratoryManagment of Acute Respiratory FailureFailure Pharmacological, Noninvasive &Pharmacological, Noninvasive & InvasiveInvasive Dafsah Arifa JuzarDafsah Arifa Juzar Cardiac Intensivist & Interventional CardiologistCardiac Intensivist & Interventional Cardiologist Working Group Acute & Intensive CardiovascularWorking Group Acute & Intensive Cardiovascular CareCare
- 2. Acute respiratory failure occurs when dysfunction of the respiratory system results in abnormal gas exchange that is potentially life-threatening. Acute implies a relatively sudden onset (from hours to days) and a substantial change from the patient's baseline condition Respiratory failure is a failure of the process of delivering O2 to the tissues and/or removing CO2 from the tissues.
- 3. Penyebab utamaPenyebab utama HipoksemiaHipoksemia V/Q mismatch < 1V/Q mismatch < 1 • acute lung oedema of any cause, Pneumoniaacute lung oedema of any cause, Pneumonia and pulmonary embolismand pulmonary embolism Alveolar hypoventilation - induce PACOAlveolar hypoventilation - induce PACO22 increase and decrease in PaOincrease and decrease in PaO22.. • COPD, comatose pts., drug poisoningCOPD, comatose pts., drug poisoning
- 4. History/ examinationHistory/ examination Chest X - rayChest X - ray EchocardiogramEchocardiogram Blood ChemistryBlood Chemistry ECGECG Oxygen saturationOxygen saturation Full blood countFull blood count Suspected Acute Heart FailureSuspected Acute Heart Failure SimultaneouslySimultaneously asses forasses for UrgentUrgent actionaction if presentif present Life-threateningLife-threatening arrhythmiaarrhythmia bradycardiabradycardia Blood pressureBlood pressure <85 mmhg<85 mmhg or shockor shock AcuteAcute CoronaryCoronary SyndromeSyndrome AcuteAcute mechanicalmechanical cause/severecause/severe valvular diseasevalvular disease •ElectricalElectrical cardioversioncardioversion •pacingpacing •Inotropes/Inotropes/ •vasopresorvasopresor •mechanicalmechanical circulatorycirculatory supportsupport (e.g. IABP)(e.g. IABP) •CoronaryCoronary •reperfusionreperfusion •AntithromboticAntithrombotic •therapytherapy •EchoEcho •surgical/ PCIsurgical/ PCI •OXYGENOXYGEN •NIVNIV •ETT &ETT & INVASIVEINVASIVE VENTILATIONVENTILATION Ventilation/Ventilation/ SystemicSystemic oxygenationoxygenation inadequateinadequate ESC guidelines. Eur Heart J 2012ESC guidelines. Eur Heart J 2012
- 5. Sistim respirasiSistim respirasi Kunci penangan kegagalan KVKunci penangan kegagalan KV Perubahan sistem respirasi berdampak padaPerubahan sistem respirasi berdampak pada haemodynamic.haemodynamic. Ventilasi mekanik, bila diperlukanVentilasi mekanik, bila diperlukan menguntungkanmenguntungkan berdampak negatif terhadap fungsi KVberdampak negatif terhadap fungsi KV
- 6. COCO↓↓ LV pressureLV pressure↑↑ PeripheralPeripheral hypoperfusionhypoperfusion WedgeWedge pressurepressure↑↑↑↑ WedgeWedge pressurepressure↑↑↑↑ ReducedReduced OxygenationOxygenation PulmonaryPulmonary EdemaEdema PulmonaryPulmonary EdemaEdema RespiratoryRespiratory failurefailure RVRV failurefailure MyocardialMyocardial ischemiaischemia ++ Afterload mismatchAfterload mismatchAfterload mismatchAfterload mismatch SVRSVR ↑↑SVRSVR ↑↑LVLV ↓↓ contractilitycontractility LVLV ↓↓ contractilitycontractility Neurohormonal &Neurohormonal & Inflammatory activationInflammatory activation Neurohormonal &Neurohormonal & Inflammatory activationInflammatory activation DecreasedDecreased FluidFluid clearanceclearance DecreasedDecreased FluidFluid clearanceclearance AlveolarAlveolar ↑↑ CapillaryCapillary permeabilitypermeability AlveolarAlveolar ↑↑ CapillaryCapillary permeabilitypermeability
- 7. Pulmonary EdemaPulmonary Edema Shunt, HypoxiaShunt, Hypoxia ComplianceCompliance ResistanceResistance ACUTEACUTE HEART FAILUREHEART FAILURE Work ofWork of BreathingBreathing Diaphragm VODiaphragm VO22 AfterloadAfterload PreloadPreload MVOMVO22 IntrathoracicIntrathoracic pressurepressure Autoagravation betweenAutoagravation between Respiratory & Heart FailureRespiratory & Heart Failure Adapted Ducros L. Acute Heart Failure. SpringerAdapted Ducros L. Acute Heart Failure. Springer 20082008
- 8. Kegagalan Pernafasan AkutKegagalan Pernafasan Akut Acute Respiratory FailureAcute Respiratory Failure butuh bantuan ventilasibutuh bantuan ventilasi NIV: CPAP VS NIPSVNIV: CPAP VS NIPSV kriteria NIV (-)kriteria NIV (-) PaO2/FiO2 < 145PaO2/FiO2 < 145 APACHE II > 34APACHE II > 34 GCS < 11GCS < 11 Kontraindikasi NIVKontraindikasi NIV PS 8-10 cmHPS 8-10 cmH22OO PEEP 4-5 cmHPEEP 4-5 cmH22OO 60 menit60 menit
- 9. Figure 23.3 Pressure–time curves. Spontaneous breathing, CPAP (10 cmH2O) and bilevel pressure support (IPAP 22Figure 23.3 Pressure–time curves. Spontaneous breathing, CPAP (10 cmH2O) and bilevel pressure support (IPAP 22 cmH2O, EPAP 10 cmH2O) with pressure support (PS) 12 cmH2O.cmH2O, EPAP 10 cmH2O) with pressure support (PS) 12 cmH2O. Josep Masip, Kenneth PlanasThe ESC Textbook of Intensive and Acute Cardiac Care: Noninvasive ventilationJosep Masip, Kenneth PlanasThe ESC Textbook of Intensive and Acute Cardiac Care: Noninvasive ventilation © European Society of Cardiology© European Society of Cardiology
- 10. PemantauanPemantauan Interpertasi gagal nafas secara akuratInterpertasi gagal nafas secara akurat Polypnoe, sianosis, takikardia dan intercostal,Polypnoe, sianosis, takikardia dan intercostal, suprasternal dan supraclavicular.suprasternal dan supraclavicular. Sat O2 -plethysmography (kecuali akral dingin)Sat O2 -plethysmography (kecuali akral dingin) tanda - tanda hiperkapniatanda - tanda hiperkapnia • berkeringat, flapping tremor dan penurunanberkeringat, flapping tremor dan penurunan kesadarankesadaran Analisa gas darah akan konfirmasi penilaian klinisAnalisa gas darah akan konfirmasi penilaian klinis
- 11. Indikasi & KontraindikasiIndikasi & Kontraindikasi NIVNIV IndikasiIndikasi KontraindikasiKontraindikasi Pemeriksaan fisikPemeriksaan fisik AbsoluteAbsolute dyspnea sedang - beratdyspnea sedang - berat Henti jantung atau pernafasanHenti jantung atau pernafasan takipneatakipnea hipoksia refrakterhipoksia refrakter •Usaha nafas yang meningkat,Usaha nafas yang meningkat, otot tambahan, perrnafasan abdomialotot tambahan, perrnafasan abdomial paradoksparadoks abnormalitas anatomi fasialisabnormalitas anatomi fasialis Pertukaran gasPertukaran gas syok tidak segera tertanganisyok tidak segera tertangani gagal nafas : hipercapnia asidosisgagal nafas : hipercapnia asidosis RelatifRelatif HipoksemiaHipoksemia hipotensi ringanhipotensi ringan pasien agitasi dan tidak koperatifpasien agitasi dan tidak koperatif jalan nafas tidak dapat dijalan nafas tidak dapat di pertahankanpertahankan sekresi berlebihansekresi berlebihan kegagalan multi organkegagalan multi organ
- 12. Pulmonary EdemaPulmonary Edema Shunt, HypoxiaShunt, Hypoxia ComplianceCompliance ResistanceResistance IMPROVEDIMPROVED HEART FAILUREHEART FAILURE Work ofWork of BreathingBreathing Diaphragm VODiaphragm VO22 AfterloadAfterload PreloadPreload MVOMVO22 IntrathoracicIntrathoracic pressurepressure Effect Positive Pressure Ventilation inEffect Positive Pressure Ventilation in Respiratory & Heart FailureRespiratory & Heart Failure Adapted Ducros L. Acute Heart Failure. SpringerAdapted Ducros L. Acute Heart Failure. Springer 20082008
- 13. Potensi keuntungan NIV (CPAP/NIPPV)Potensi keuntungan NIV (CPAP/NIPPV) pada AHFpada AHF Sistim OrganSistim Organ KeuntunganKeuntungan Respon KlinisRespon Klinis KardiovaskularKardiovaskular AfterloadAfterload ↓↓ PreloadPreload ↓↓ Perbaikan stroke volumePerbaikan stroke volume PulmonalPulmonal ↑↑ airway complianceairway compliance ↑↑ aveolar recruitmentaveolar recruitment ↓↓ pulmonary shuntpulmonary shunt Perbaikan oksigenasiPerbaikan oksigenasi work of breathingwork of breathing ↓↓ NeurohormonalNeurohormonal ↓↓ cardiac adrenergiccardiac adrenergic activityactivity ↓↓ endothelin-1endothelin-1 expressionexpression HR and BPHR and BP ↓↓
- 14. IndikasiIndikasi Gagal NapasGagal Napas • Apnea / Respiratory ArrestApnea / Respiratory Arrest • Ventilasi tidak adekwat (akut vs. kronik)Ventilasi tidak adekwat (akut vs. kronik) • Oxygenasi tidak adekwatOxygenasi tidak adekwat DisfungsiDisfungsi JantungJantung • Mengurangi/ eliminasi “work of breathing”Mengurangi/ eliminasi “work of breathing” • Mengurangi Konsumsi oksigenMengurangi Konsumsi oksigen DisfungsiDisfungsi NeurologiNeurologi • Hipoventilasi sentral / apnea berulangHipoventilasi sentral / apnea berulang • Pasien comatose, GCSPasien comatose, GCS << 88 • Tidak mampu mempertahankan jalan napasTidak mampu mempertahankan jalan napas
- 15. Kegagalan Pernafasan AkutKegagalan Pernafasan Akut Acute Respiratory FailureAcute Respiratory Failure butuh bantuan ventilasibutuh bantuan ventilasi NIV: CPAP VS NIPSVNIV: CPAP VS NIPSV KriteriaKriteria intubasiintubasi kriteria NIV (-)kriteria NIV (-) PaO2/FiO2 < 145PaO2/FiO2 < 145 APACHE II > 34APACHE II > 34 GCS < 11GCS < 11 Kontraindikasi NIVKontraindikasi NIV PS 8-10 cmHPS 8-10 cmH22OO PEEP 4-5 cmHPEEP 4-5 cmH22OO
- 16. OO22COCO22 CPAPCPAP Non Invasive VentilationNon Invasive Ventilation
- 17. OO22COCO22 Non Invasive VentilationNon Invasive Ventilation NIPSVNIPSV
- 18. Prediktor kegagalan terapi NIVPrediktor kegagalan terapi NIV pada kegagalan respirasi akutpada kegagalan respirasi akut UMUMUMUM Setelah 60 menitSetelah 60 menit pernafasan asinkron denganpernafasan asinkron dengan ventilatorventilator RR tidak turunRR tidak turun Kebocoran udaraKebocoran udara pH tidak ada perbaikanpH tidak ada perbaikan Sekresi banyakSekresi banyak Oksigenasi tidak ada perbaikanOksigenasi tidak ada perbaikan RR sangat tinggiRR sangat tinggi CO2 tidak ada perbaikanCO2 tidak ada perbaikan secara subyektif toleransi tidak baiksecara subyektif toleransi tidak baik Gangguan neurologisGangguan neurologis ALI/ ARDSALI/ ARDS Asidosis metabolikAsidosis metabolik Hipoksemia berat dengan terapiHipoksemia berat dengan terapi oksigenoksigen syoksyok berat keadaan umum tinggiberat keadaan umum tinggi
- 19. NIPSVNIPSV
- 20. CPAPCPAP Initiation of TreatmentInitiation of Treatment Start 5 cm HStart 5 cm H22OO Studies demonstrated beneficial effectStudies demonstrated beneficial effect 7.5 cmH7.5 cmH22O & 12.5 cmHO & 12.5 cmH22OO Upward titration increment 2 cm HUpward titration increment 2 cm H22OO No guidelines exist regarding duration of CPAP therapyNo guidelines exist regarding duration of CPAP therapy In ACPE, response CPAP was evaluated 6 - 48 hours, withIn ACPE, response CPAP was evaluated 6 - 48 hours, with improvement seen in the 1st hour.improvement seen in the 1st hour. ACPE : Acute cardiogenic pulmonary edemaACPE : Acute cardiogenic pulmonary edema
- 21. CPAPCPAP WeaningWeaning Once desired effect achieved weaned off in theOnce desired effect achieved weaned off in the manner similar to initial uptitrationmanner similar to initial uptitration
- 22. NIPSVNIPSV Initiation of TreatmentInitiation of Treatment Bilevel NPPVBilevel NPPV IPAPIPAP (PSV)(PSV) = 8 – 12 cmH= 8 – 12 cmH22OO EPAPEPAP (CPAP)(CPAP) = 3 – 5 cmH= 3 – 5 cmH22OO ∆∆ Ventilation =Ventilation = ∆∆ IPAPIPAP ∆∆ Oxygenation =Oxygenation = ∆∆ EPAPEPAP
- 23. NIPSVNIPSV Initiation of TreatmentInitiation of Treatment If noIf no ↓↓ in dyspnea or respiratory rate, thenin dyspnea or respiratory rate, then ↑↑ IPAP 2-3 cmHIPAP 2-3 cmH22OO Maximum IPAP = 20 – 25 cmHMaximum IPAP = 20 – 25 cmH22OO If hypoxemia present,If hypoxemia present, ↑↑ EPAP in 2 – 3 cmHEPAP in 2 – 3 cmH22OO incrementsincrements Maximum EPAP = 15 cmHMaximum EPAP = 15 cmH22OO
- 24. NIPSVNIPSV WeaningWeaning ProgressiveProgressive ↓↓ in level of IPAP/EPAPin level of IPAP/EPAP Once low level of NPPV tolerated -Once low level of NPPV tolerated - ∅∅ IPAP = 5 cmHIPAP = 5 cmH22OO EPAP = 5 cmHEPAP = 5 cmH22OO Progressive time off NIPSVProgressive time off NIPSV Similar to “T-piece” approachSimilar to “T-piece” approach
- 25. NIPSVNIPSV ComplicationsComplications Potential for rebreathing and PaCOPotential for rebreathing and PaCO22 retentionretention with bilevel NPPVwith bilevel NPPV Single limb circuit – no exhalation valveSingle limb circuit – no exhalation valve System has fixed leak in circuitSystem has fixed leak in circuit Mask shouldMask should notnot have air-tight sealhave air-tight seal Maintain CPAP of at least 4 - 5 cmHMaintain CPAP of at least 4 - 5 cmH22OO
- 26. NIPSVNIPSV ComplicationsComplications Aspiration - < 5%Aspiration - < 5% Limit IPAP < 20 – 25 cmHLimit IPAP < 20 – 25 cmH22OO NGT if above pressures neededNGT if above pressures needed Most commonMost common Skin irritationSkin irritation Eye irritationEye irritation
- 28. 1 Winck JC etal. Crit Care. 2006;10(2):R69.1 Winck JC etal. Crit Care. 2006;10(2):R69. 2 Masip J etal. JAMA. 2005 Dec2 Masip J etal. JAMA. 2005 Dec 28;294(24):3124-30.28;294(24):3124-30. 3 Peter JV etal. Lancet. 2006 Apr3 Peter JV etal. Lancet. 2006 Apr 8;367(9517):1155-63.8;367(9517):1155-63. NETINETI MORTALITASMORTALITAS Risk for MyocardialRisk for Myocardial infarctioninfarction 11 ARRARR 22 ITTITT analysisanalysis reductionreduction 33 RRRR 11 22 RelativeRelative RiskRisk ReductionReduction 33 RRRR 11 22 33 CPAP vsCPAP vs SMTSMT -22%-22% 60%60% 0.400.40 -13%-13% 46%46% 0.590.59 -- -- -- NIPSV vsNIPSV vs SMTSMT -18%-18% 49%49% 0.500.50 -7%-7% 37%37% NSNS -- -- -- NIPSV vsNIPSV vs CPAPCPAP -3% (NS)-3% (NS) NSNS NSNS -2% (NS)-2% (NS) NSNS NSNS NSNS NSNS ARR : absolute risk reductionARR : absolute risk reduction ITT : Intention to treatITT : Intention to treat RR : Relative ReductionRR : Relative Reduction NS : non significantNS : non significant NIV Meta AnalysisNIV Meta Analysis
- 29. NIPSV & CPAPNIPSV & CPAP ESC Heart Failure Guidelines 2005 & 2008 :ESC Heart Failure Guidelines 2005 & 2008 : Class IIA Recommendation.Class IIA Recommendation. Level of Evidence : ALevel of Evidence : A Should be used with caution in cardiogenic shock & right heart failureShould be used with caution in cardiogenic shock & right heart failure
- 30. OO22COCO22
- 31. Seting AwalSeting Awal SettingsSettings VCVC VT 10-12 cc/EBB (8 cc/EBB)VT 10-12 cc/EBB (8 cc/EBB) Rate: 10-15Rate: 10-15 (sesuaikan dengan MV pre)(sesuaikan dengan MV pre) FiOFiO22: 100%, di sapih sat 02 perifer: 100%, di sapih sat 02 perifer PEEP: 5-7PEEP: 5-7 PPplateauplateau < 30 cmH< 30 cmH22OO
- 32. Suara Nafas bilateralSuara Nafas bilateral Vital sign & haemodynamic valuesVital sign & haemodynamic values Analisa gas darah (AGD), dinilai 20-30 menitAnalisa gas darah (AGD), dinilai 20-30 menit setelah inisiasi ventilasi mekaniksetelah inisiasi ventilasi mekanik pH 7.35 - 7.45pH 7.35 - 7.45 PaCO2 35-45 mmhgPaCO2 35-45 mmhg PaO2 60 -100 mmhg (Sat O2 > 95-99 %)PaO2 60 -100 mmhg (Sat O2 > 95-99 %)
- 33. PemantauanPemantauan Optimalisasi setting respirator (TV, RR, PEEP, etc)Optimalisasi setting respirator (TV, RR, PEEP, etc) Hindari tekanan airway yang berlebihanHindari tekanan airway yang berlebihan Minimalisasikan efek negatif dari tekanan positifMinimalisasikan efek negatif dari tekanan positif ventilasi terhadap hemodinamik.ventilasi terhadap hemodinamik. Optimalkan tatalaksana respirasi.Optimalkan tatalaksana respirasi.
- 34. Pressure vs. VolumePressure vs. Volume Pressure LimitedPressure Limited FiOFiO22 and MAPand MAP (oksigenasi) dikontrol(oksigenasi) dikontrol Still can influenceStill can influence ventilation somewhatventilation somewhat (respiratory rate, PAP)(respiratory rate, PAP) Pola flow patternPola flow pattern seselerasi (PIP <seselerasi (PIP < untuk TV yang sama)untuk TV yang sama) Volume Limited • “minute ventilation” dikontrol • Oksigenasi dapat dipengaruhi dengan (FiO2, PEEP, I-time) • “flow pattern” gelombangnya persegi
- 35. Pressure vs. VolumePressure vs. Volume
- 36. Pilihan OperatorPilihan Operator Pressure LimitedPressure Limited FiOFiO22 RateRate I-timeI-time PEEPPEEP – PIPPIP •Volume Limited – FiO2 – Rate – Tidal Volume – PEEP – I time Tidal VolumeTidal Volume ( & MV) Variasi( & MV) Variasi PIP ( & MAP)PIP ( & MAP) VariasiVariasi MAPMAP MVMV
- 37. NomenclatureNomenclature Airway PressuresAirway Pressures Peak Inspiratory Pressure (PIP)Peak Inspiratory Pressure (PIP) Positive End Expiratory Pressure (PEEP)Positive End Expiratory Pressure (PEEP) Pressure above PEEP (PAP orPressure above PEEP (PAP or ΔΔP)P) Mean airway pressure (MAP)Mean airway pressure (MAP) Continuous Positive Airway Pressure (CPAP)Continuous Positive Airway Pressure (CPAP) Inspiratory Time or I:E ratioInspiratory Time or I:E ratio Tidal Volume:Tidal Volume: jumlah gas/ udara yang diberikan setiap nafasjumlah gas/ udara yang diberikan setiap nafas
- 39. Control vs. SIMVControl vs. SIMV Control ModesControl Modes Setiap nafas di bantuSetiap nafas di bantu tanpa memperhatikantanpa memperhatikan “trigger”“trigger” Pasien bisa hiperventilasiPasien bisa hiperventilasi bila agitasi.bila agitasi. Pasien/ vent bisa asinkroniPasien/ vent bisa asinkroni dan perlu sedasi +/-dan perlu sedasi +/- paralitikparalitik SIMV Modes • Vent berusaha sinkroni dengan usaha pasien • Pasien dapat nafas “sendiri” (+/- PS )diantaranya. • “work of breathing” bisa meningkat • Dapat terjadi pasien / vent asinkroni
- 40. TriggerTrigger Bagaimana vent mengetahui kapan harusBagaimana vent mengetahui kapan harus memberi nafas ? - “Trigger”memberi nafas ? - “Trigger” Usaha pasienUsaha pasien elapsed timeelapsed time Usaha pasien dapat rasakan sebagai perubahanUsaha pasien dapat rasakan sebagai perubahan“tekanan/Pressure” atau perubahan “aliran/flow”“tekanan/Pressure” atau perubahan “aliran/flow”dalam sirkuitdalam sirkuit
- 41. Perlu bantuan ??Perlu bantuan ?? Pressure SupportPressure Support ““Triggering” vent membutuhkan usaha nafas dariTriggering” vent membutuhkan usaha nafas dari pasien.pasien. Dapat mengurangi “work of breathing” denganDapat mengurangi “work of breathing” dengan memberikan tekanan/ pressure saat pasienmemberikan tekanan/ pressure saat pasien memberikan “trigger”memberikan “trigger”
- 42. Pertukaran Gas AbnormalPertukaran Gas Abnormal • HipoksemiaHipoksemia penyebabnya :penyebabnya : hipoventilasihipoventilasi V/Q mismatchV/Q mismatch shuntshunt Gangguan diffusiGangguan diffusi •Hipercaknia penyebabnya : – hipoventilasi – V/Q mismatch
- 43. Faktor yg mempengaruhiFaktor yg mempengaruhi Oksigen masukOksigen masuk ↑↑ FFIIOO22 ↑↑ mean alveolarmean alveolar pressurepressure PEEPPEEP Re-open alveoli andRe-open alveoli and ↓↓ shuntshunt •Carbon dioxide keluar – ↑ ventilation • ↑ RR • ↑ tidal volume
- 44. ““Mean airway pressure”Mean airway pressure” Mean airway pressureMean airway pressure Mean airway pressureMean airway pressure TimeTime PressurePressure TimeTime PressurePressure
- 45. ““Mean airway pressure”Mean airway pressure” Mean airway pressureMean airway pressure Mean airway pressureMean airway pressure TimeTime PressurePressure TimeTime PressurePressure
- 47. HypotensionHypotension HypovolaemiaHypovolaemia Positive intrathoracic pressurePositive intrathoracic pressure
- 59. HypotensionHypotension HypovolaemiaHypovolaemia DrugsDrugs Dynamic hyperinflationDynamic hyperinflation Tension pneumothoraxTension pneumothorax
- 60. High airway pressureHigh airway pressure
- 61. High airway pressureHigh airway pressure BarotraumaBarotrauma Change in patient’s conditionChange in patient’s condition Inadequate ventilationInadequate ventilation
- 62. Inappropriate settingsInappropriate settings Excessive tidal volumeExcessive tidal volume Excessive inspiratory flowExcessive inspiratory flow Excessive PEEPExcessive PEEP
- 63. 700 ml700 ml -70-70 70 l/min70 l/min High airway pressureHigh airway pressure PressurePressure FlowFlow VolumeVolume PressurePressure alarm limitalarm limit
- 64. High airway pressureHigh airway pressure ResistanceResistance ETT tubeETT tube BronchospasmBronchospasm ComplianceCompliance Lung parenchymaLung parenchyma PleuralPleural Chest wallChest wall ↓↓ Lung volumeLung volume
- 65. High airway pressureHigh airway pressure ResistanceResistance ETT tubeETT tube BronchospasmBronchospasm ComplianceCompliance Lung parenchymaLung parenchyma PleuralPleural Chest wallChest wall ↓↓ Lung volumeLung volume
- 67. High airway pressureHigh airway pressure ResistanceResistance ETT tubeETT tube BronchospasmBronchospasm ComplianceCompliance Lung parenchymaLung parenchyma PleuralPleural Chest wallChest wall ↓↓ Lung volumeLung volume
- 68. High airway pressure •Resistance – ETT tube – Bronchospasm •Compliance – Lung parenchyma – Pleural – Chest wall – ↓ Lung volume
- 70. DysynchronyDysynchrony AgitationAgitation Look for and treat causeLook for and treat cause Mode of ventilationMode of ventilation Spontaneous vs SIMV vs Assist controlSpontaneous vs SIMV vs Assist control BIPAPBIPAP I:E ratioI:E ratio TriggeringTriggering FlowFlow PressurePressure Auto-PEEPAuto-PEEP
- 72. DesaturationDesaturation Endobronchial intubationEndobronchial intubation Accidental extubation/disconnectionAccidental extubation/disconnection Ventilator failureVentilator failure Oxygen failureOxygen failure All causes of hypoxic respiratory failureAll causes of hypoxic respiratory failure Pulmonary embolusPulmonary embolus PneumothoraxPneumothorax
- 73. PenyapihanPenyapihan Weaning/ PenyapihanWeaning/ Penyapihan Apakah penyebab gagal napas sudah teratasiApakah penyebab gagal napas sudah teratasi atau sudah perbaikan?atau sudah perbaikan? Apakah oksigenasi dan ventilasi pasien baik?Apakah oksigenasi dan ventilasi pasien baik? Apakah jantung mampu mentoleransiApakah jantung mampu mentoleransi peningkatan work of breathing ?peningkatan work of breathing ?
- 74. PenyapihanPenyapihan Weaning (samb.)Weaning (samb.) Kurangi PEEP (4-5)Kurangi PEEP (4-5) Kurangi rateKurangi rate Kurangi PIP (seperlunya)Kurangi PIP (seperlunya) Apa yang ingin anda kerjakan adalahApa yang ingin anda kerjakan adalah mengurangi apa yang dikerjakan danmengurangi apa yang dikerjakan dan perhatikan apakah pasien dapat mengatasiperhatikan apakah pasien dapat mengatasi perubahannya ….perubahannya ….
- 75. Metoda PenyapihanMetoda Penyapihan Bantuan ventilatorBantuan ventilator penuh (VC/SIMV/PC)penuh (VC/SIMV/PC) Partial ventilatorPartial ventilator (SIMV +PS, PS)(SIMV +PS, PS) PernafasanPernafasan spontanspontan (T-piece, CPAP)(T-piece, CPAP) EktubasiEktubasi
- 76. EkstubasiEkstubasi EkstubasiEkstubasi Refleks saluran nafas baik (batuk)Refleks saluran nafas baik (batuk) Saluran nafas atas paten ?Saluran nafas atas paten ? Kebutuhan oksigen minimalKebutuhan oksigen minimal rate minimalrate minimal Pressure support minimal (0-10)Pressure support minimal (0-10) Pasien “sadar/ bangun”Pasien “sadar/ bangun”
- 77. ““Check list”Check list” pasien ekstubasipasien ekstubasi KriteriaKriteria RespirasiRespirasi • PaO2PaO2 >>60 mmhg on FiO260 mmhg on FiO2 << 40-50% &40-50% & PEEPPEEP << 5-85-8 • PCO2 normalPCO2 normal • Pasien dapat usaha inspirasiPasien dapat usaha inspirasi KriteriaKriteria KardiovaskularKardiovaskular • Tidak ada bukti iskemia miokardTidak ada bukti iskemia miokard • HRHR << 140 bpm140 bpm • BP normal w/o vasopressor atauBP normal w/o vasopressor atau rendah (doparendah (dopa << 5 mmhg)5 mmhg) Mental StatusMental Status • Bangun, GCSBangun, GCS >> 1313 ComorbidComorbid • Pasien afebrisPasien afebris • Elektrolit normalElektrolit normal
- 78. Identifikasi pasien yangIdentifikasi pasien yang toleransi SBTtoleransi SBT PengukuranPengukuran Dewasa NDewasa N AmbangAmbang keberhasilankeberhasilan VVTT 5-7 L/mnt5-7 L/mnt 4-6 L/mnt4-6 L/mnt RRRR 10 - 18 x/mnt10 - 18 x/mnt 30 - 38 x/mnt30 - 38 x/mnt RR/VRR/VTT rasiorasio 40 -50/L40 -50/L 60 -105/L60 -105/L
- 79. Kegagalan Pernafasan AkutKegagalan Pernafasan Akut Acute Respiratory FailureAcute Respiratory Failure butuh bantuan ventilasibutuh bantuan ventilasi NIV: CPAP VS NIPSVNIV: CPAP VS NIPSV KriteriaKriteria intubasiintubasi Intubasi ETIntubasi ET Ventilasi mekanikVentilasi mekanik Sinkroni yg adekwatSinkroni yg adekwat perbaikan usaha pernafasanperbaikan usaha pernafasan perbaikan pertukaran Gasperbaikan pertukaran Gas kriteria NIV (-)kriteria NIV (-) PaO2/FiO2 < 145PaO2/FiO2 < 145 APACHE II > 34APACHE II > 34 GCS < 11GCS < 11 Kontraindikasi NIVKontraindikasi NIV PS 8-10 cmHPS 8-10 cmH22OO PEEP 4-5 cmHPEEP 4-5 cmH22OO 60 menit60 menit FiOFiO22 < 40%< 40% SpOSpO22 > 90%> 90% PerbaikanPerbaikan pernafasanpernafasan ““Weaning”Weaning” ExtubasiExtubasi SulitSulit ““Weaning”Weaning” NIV weaningNIV weaning NIV PaliatifNIV Paliatif
- 81. MODALITAS PENANGANANMODALITAS PENANGANAN GAGAL JANTUNG AKUTGAGAL JANTUNG AKUT
- 85. Milestones of Mechanical Ventilation Impending RespiratoryImpending Respiratory FailureFailure InterventionsInterventions ∀NPPVNPPV ∀ChestChest PhysiotherapyPhysiotherapy ∀BronchodilatorsBronchodilators ∀ ExtubationExtubation GapGap InterventionsInterventions ∀ NPPVNPPV ∀Chest PhysiotherapyChest Physiotherapy ∀BronchodilatorsBronchodilators ∀ TrialTrial GapGap •AdjunctsAdjuncts •ModesModes Atasi gagal janutngAtasi gagal janutng PhysiotherapyPhysiotherapy BronchodilatorsBronchodilators ProningProning ∀ StabilizationStabilization WeaningWeaning IntubationIntubation PointPoint • Hemodynamic StabilityHemodynamic Stability • PIPPIP << 25 V25 Vtt ⇔⇔ 10 cc/kg10 cc/kg • FiOFiO22 << 40%40% • PEEPPEEP << 55 • PaOPaO22 >> 6060 • PaCOPaCO22 = 30-55= 30-55 • pH = 7.33-7.55pH = 7.33-7.55 • Intact cough/gag reflexesIntact cough/gag reflexes • No procedures in progress/pendingNo procedures in progress/pending ExtubationExtubation Trial PointTrial Point Adjust PSAdjust PS << 1010 to deliverto deliver Vt = 4 – 6 cc/kgVt = 4 – 6 cc/kg PressurePressure Support TrialSupport Trial ( 1 hour)( 1 hour) • Reliable spontaneous respiratory rateReliable spontaneous respiratory rate • Hemodynamic StabilityHemodynamic Stability • No Apnea/bradycardiaNo Apnea/bradycardia • PSPS << 1010 ⇔⇔ VVtt >> 4 - 6 cc/kg4 - 6 cc/kg • PaOPaO22 >> 6060 • PaCOPaCO22 = 30-55= 30-55 • Art pH = 7.33-7.55Art pH = 7.33-7.55 ExtubatableExtubatable PointPoint ExtubationExtubation PointPoint ExtubatedExtubated > 48 hrs> 48 hrs ReintubatedReintubated < 48 hrs< 48 hrs
Editor's Notes
- Amplification phase : Vicious cycle amplified by 4 distinct mechanism Myocardial ischemia : impaired gas exchange and hypoxia, leading to increased catecholamine production, leading to increased systemic vascular resistance and blood pressure, leading to increased myocardial wall tension and oxygen demand, leading to myocardial ischemia, leading to LV systolic and diastolic dysfunction, leading to decreased cardiac output and increased end-diastolic pressure. Further worsening pulmonary edema. RV failure : increased fluid and hypoxia increase PA resistance translated increase RV pressure again compromising LV function Respiratory failure : decreased oxygenation acidemia reduced cardiac output lead to central respiratory drive depression leakage aveolar-capillary membrane and decreased alveolar fluid resistance: hypoxia & inflamation therefore, at its most basic level, the end result of this cycle is to have an LV trying in vain to pump against a markedly elevated systemic vascular resistance (increased afterload), resulting in poor cardiac output. This cycle eventually results in florid pulmonary edema, hypoxia, and respiratory failure unless the cycle is terminated.
- Patients are often (ideally) intubated before they reach the point of respiratory failure. Respiratory distress can be due to inadequate ventilation, oxygenation or a combination thereof. The process can be either intrinsic to the lungs (pneumonia, for example) or to the chest wall (“pump failure”, as in muscular dystrophies). For some patients, the work of breathing may be such that they are unable to gain weight even in the face of adequate ventilation and oxygenation.
- The function of the ventilator is to help get oxygen into the patient and carbon dioxide out
- The function of the ventilator is to help get oxygen into the patient and carbon dioxide out
- WINC JC PETER JV In patients with acute cardiogenic pulmonary oedema, CPAP and bilevel ventilation reduces the need for subsequent mechanical ventilation. Compared with standard therapy, CPAP reduces mortality; our results also suggest a trend towards reduced mortality after bilevel NIPPV.
- Based Mehta 97 & Rusterholtz 99, increased incidence of myocardial infarction tapi penelitian baru Kelly 2002 & Marcip 2000 & Bellone 2004
- The function of the ventilator is to help get oxygen into the patient and carbon dioxide out
- The starting breath rate is usually one that would be physiologically appropriate for the patient. The starting number may be increased or decreased as dictated by the clinical situation. Immediately after intubation, patients are placed on an FiO2 of 100% (1.00 to be accurate). This can be weaned down as long as the oxygen saturation remains acceptable. PEEP usually is set at 5 mmH2O and then increased as needed to achieve acceptable oxygen saturation with a FiO2 &lt;0.6. In some cases (asthma, head trauma), the PEEP may be set at 3 mmH2O to start. Most patients are started off in an SIMV mode. If their clinical situation worsens, the mode may be changed to assist control to decrease their work of breathing and give the clinician more precise control over ventilatory function.
- PRESSURE-LIMITED I would not say that I have limited ability to affect ventilation in PC, though I may choose to increase the PAP recognizing that I accept the potential for increased baro/volutrauma at the same time I also accept that I may suffer a decrease in ventilation with changes in compliance. VOLUME-LIMITED Accept that changes in compliance may lead to increases in peak airway pressures and associated baro/volutrauma.
- The decision to choose volume or pressure as a mode is based on what the clinician is more interested in directly affecting. Volume modes offer a guaranteed minute ventilation while pressure modes allow one to directly manipulate the MAP. In infants less than 5-10 kgs., pressure modes are usually chosen due to the inability of the ventilator to give small volumes (&lt;50 cc) accurately.
- These are some of the basic terms used with ventilators. CPAP is equivalent to PEEP except the term is usually used when referring to patients who are not intubated (i.e., on nasal CPAP).
- Control modes are used when complete control over the patient’s ventilation and/or oxygenation is desired. This is usually because the patient’s lung disease is significant enough that you that you wish to give maximal support. Another scenario may be one in which you want to precisely control the PaCO2, as in hyperventilation for increased intracranial pressure. Patients placed on control modes are often deeply sedated and may be given neuromuscular blockers. SIMV modes are chosen when you want the patient to do as much work as they can tolerate and try to minimize the support from the ventilator. SIMV modes are used to wean patients; as you decrease the set rate, the patient will need to do more on their own to maintain normal blood gases. In control modes, if you decrease the rate, the patient’s spontaneous efforts will be fully supported so you will not know how much of that particular tidal volume they are generating on their own. Note that for the paralyzed patient there is no significant difference between assist control and SIMV.
- Ventilators deliver breaths when they are told to do so. This occurs when a certain amount of time has elapsed (e.g., 5 seconds if the rate is 12 [60 sec/12 b/m = 5 sec]) or when the patient makes an effort. A patient’s effort may be sensed as a change in pressure in the circuit (negative deflection) or as a change in flow (also a negative deflection). Flow sensors tend to have a more rapid response time. The amount of support delivered with a patient triggered breath will depend on the mode (assist control vs. IMV vs. SIMV) and the amount of pressure support that is set.
- A patient needs to generate a certain amount of work in order to trigger it. Additionally, a patient has to breathe through an ETT that is almost always narrower than their own airway and ventilate the increased dead space imposed by the vent circuit. A patient may not be able to generate adequate tidal volumes for these reasons. To compensate for this increase in the work of breathing, pressure support is given. The ventilator generates pressure support by adding flow to the circuit during patient-triggered breaths in IMV or SIMV modes. This does not make it easier for the patient to trigger the ventilator but it does help the patient generate larger tidal volumes. Pressure support usually terminates when the flow in the circuit is 25% of the peak flow.
- As ventilator technology has advanced, newer modes have been developed. Some are variations of volume or pressure modes and some are completely unrelated to conventional mechanical ventilation. It is important to recognize that none of these modes have been shown to be better than another or to reduce mortality for any disease.
- As outlined in the preceding slides, hypoxemia (not hypoxia) can be the result of hypoventilation (not enough delivered) or not matching the delivery to the loading sites (V/Q mismatch). Shunt, whether intracardiac or intrapulmonary, is the ultimate form of V/Q mismatch (V/Q =∞ ). Diffusion impairments must be significant to result in hypoxemia and are rarely of clinical relevance in pediatrics. Hypoventilation is the primary cause of hypercarbia. V/Q mismatch must be profound before hypercarbia results for the reasons discussed in the previous slide.
- In summary, the most important means of improving oxygenation are increasing the inspired concentration of oxygen, increasing the mean airway and therefore the mean alveolar pressure and applying PEEP to re-open alveoli. Carbon dioxide removal can be increased by increasing the respiratory rate or tidal volume
- Airway pressure can be increased in a number of ways. It is easier to understand why these methods increase mean pressure if one remembers that the mean airway pressure refers to the mean across the entire respiratory cycle, both inspiration and expiration. The most obvious method of increasing the pressure is to increase the tidal volume but this will also increase the peak and plateau airway pressures and therefore increase the chance of ventilator induced lung injury.
- Prolonging the inspiratory time increases the mean pressure without increasing the peak pressure
- One of the major causes of hypotension following initiation of mechanical ventilation is relative hypovolaemia. This is revealed when the positive intrathoracic pressure resulting from mechanical ventilatiion further reduces venous return and hence cardiac output. [hypotension02]
- The problem is further exacerbated by the vasodilatory and myocardial depressant effects of drugs used to induce anaesthesia and allow intubation and ventilation. Fortunately these effects are usually short lived and in most cases the hypotension responds to fluid infusion [hypotension03]
- Dynamic hyperinflation due to gas trapping is a less common but nevertheless important cause of hypotension [hypotension04]
- Gas trapping occurs if there is insufficient time for alveoli to empty before the next breath [hypotension05]
- And may occur as a result of over-enthusiastic manual ventilation of the patient. It is more common in patients with asthma or chronic obstructive airways disease who have an obstruction to expiratory flow. [hypotension06]
- The net result is progressive hyperinflation of the lung with a corresponding increase in pleural pressure. This results in a fall in venous return and if severe enough can result in cardiac arrest. The simplest way of diagnosing and treating this problem is to disconnect the patient from the ventilator. The diagnosis is confirmed by an immediate rise in blood pressure. [hypotension07]
- Finally, always consider the possibility of tension pneumothorax. Although this is a relatively rare cause of hypotension following the initiation of mechanical ventilation it is important not to miss this diagnosis as it is both life-threatening and easily treated by needle thoracostomy.[hypotension08][return]
- High airway pressure is an important problem because of the risk of the barotrauma, because the development of high airway pressure indicates a deterioration in the patient’s condition and because it may lead to inadequate ventilation [paw02]
- In addition the baseline pressure, which is the PEEP, will also affect airway pressure [paw11]
- With most ventilators the ventilator inspiration is terminated if the airway pressure reaches the set upper pressure limit. As this usually occurs relatively early in inspiration this results in the patient receiving a much lower tidal volume. This is illustrated on this slide. The first 2 breaths are normal volume control breaths [paw03] On the subsequent breaths the airway pressure reaches the pressure alarm limit causing the ventilator to terminate inspiration with a resultant fall in airway pressure [paw04]and reduction in tidal volume. [paw05]
- High resistance may be due to kinking or blockage of the ET tube or due to bronchospasm while low compliance may be due to decreased parenchymal compliance due to parenchymal disease [paw15]
- Decreased pleural compliance, for example [paw16]
- Due to a pneumothorax [paw17]
- Decreased chest wall compliance, for example due to the patient fighting the ventilator [paw18]
- Or decreased ventilated lung volume, for example due to a lobar collapse [paw19]
- There are a large number of causes of patient-ventilator dysynchrony which need to be considered. It is important to identify and treat these causes and not simply to sedate the patient more heavily. As well as all the possible causes of agitation there are a number of ventilator parameters which must be considered. These include the mode of ventilation, the I:E ratio and the mode of triggering. In general spontaneous modes are more comfortable than control modes and there is some evidence that big I BIPAP is more comfortable and improves synchrony. The I:E ratio is also important with I:E ratios that are similar to the 1:2 ratio of a normal breathing pattern being more comfortable. Flow triggering tends to result in greater synchrony than pressure triggering and in general a more sensitive trigger setting is better. If the patient is having difficulty triggering the ventilator despite a sensitive setting consider the possibility that auto-PEEP due to dynamic hyperinflation is the problem.
- If no easily reversible cause for dysynchrony can be found it may be necessary to increase sedation [dysynchrony03]
- If a patient desaturates while on a mechanical ventilator it is important to consider both patient causes and equipment causes. Increase the inspired oxygen concentration to 100% and quickly check that the patient’s chest is still moving before going on to a more detailed examination. Patient causes include all causes of hypoxic respiratory failure but special consideration should be given to the possibility of pulmonary embolus and pneumothorax. [desaturation]
- In truth, you are always weaning a patient in the sense that you are always trying to minimize the ventilator settings. “True” weaning implies a different expectation - that the patient is improving and will soon not need mechanical ventilation. This usually happens when the disease process is improving or resolved and the patient has acceptable parameters. It is important to assess the ability of the heart to handle the increased demands that extubation may place upon it (e.g., pneumonia/ARDS has resolved but significant septic shock with cardiovascular collapse is present).
- Weaning is really the transfer of demands from the ventilator to the patient. By decreasing the rate, the FiO2 and the PEEP, you are asking the patient to do more. The rate at these parameters are decreased will often depend on the acuity of the disease process. The patient who was intubated because of sedation secondary to a drug overdose may wean rapidly when they are awake as compared to the child recovering from ARDS who may take weeks to completely wean from mechanical ventilatory support. The rate can be decreased in increments of 2-5 breaths/minute (or more) as dictated by the clinical situation. An arterial blood gas or end tidal CO2 monitor can be used to assess the PaCO2 after these changes. PEEP is generally lowered in increments of 1-2 mmH2O per change. As changes in oxygenation or ventilation may not be immediately apparent after a decrease in PEEP, these changes are not made more often than every 6-8 hours. [fair statement?]
- When is a patient ready to be extubated? First, they must be able to protect their airway. They should have an acceptable SaO2 on an FiO2 of no more than .30-.35. They should be breathing at a comfortable rate with a set ventilator rate of 5-8. Patients may be trialed on just pressure support/CPAP to make sure they are generating an adequate spontaneous minute ventilation. The amount of pressure support should be just enough to compensate for the added work of breathing imposed by the vent and ETT. The PEEP should be at 5 mmH2O. If these are the circumstances, then the patient is ready for an attempt at extubation and their time on mechanical ventilation (and this presentation) has come to an end.