Presentation on theme: "NON-INVASIVE VENTILATION IN ACUTE RESPIRATORY FAILURE"— Presentation transcript:
1NON-INVASIVE VENTILATION IN ACUTE RESPIRATORY FAILURE Virginia Chung, MDChief, Pulmonary & Critical Care MedicineJacobi Medical CenterJanuary 30, 2013
2OUTLINE Acute respiratory failure NIPPV / NIV / BPAP / BiPAP vs CPAP Definitions, PathophysiologyNIPPV / NIV / BPAP / BiPAP vs CPAPIndications / ContraindicationsUse of NIV in:COPD, Severe Asthma, CAP, ARDS, APE/CHF, DNI/DNRSummary of Recommendations
3BACKGROUNDRespiratory failure is a syndrome where the respiratory system fails in one or both of its gas exchange functions: oxygen uptake and carbon dioxide elimination.Respiratory failure may be acute or chronic.While acute respiratory failure (ARF) is characterized by life- threatening derangements in ABGs and acid-base status, manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.
4CLASSIFICATIONRespiratory failure can be classified as HYPOXEMIC or HYPERCAPNIC and may be ACUTE or CHRONIC.TYPE I : Hypoxemic Respiratory Failure is characterized by a PaO2 < 60 mmHg with a normal or low PaCO2.Most common form of respiratory failureCan be associated with virtually all acute diseases of the lungExamples: pulmonary edema, pneumonia, ARDS, PE
5CLASSIFICATIONTYPE II : Hypercapnic respiratory failure is characterized by a PaCO2 of > 50 mmHg.Hypoxemia is common in patients with Type II failure who are breathing room air.pH depends on the serum bicarbonate level, which, in turn, is dependent on the duration of the hypercapniaExamples: opiate overdose, neuromuscular disease, status asthmaticus, severe COPD.
6Acute vs. Chronic Hypercapnic Respiratory Failure Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH < 7.3.Chronic hypercapnic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in serum bicarbonate concentration; pH is only slightly decreased.
7PATHOPHYSIOLOGY Hypoxemic Respiratory Failure Hypoxemia can be caused by any one of these four mechanisms: Ventilation-Perfusion (V/Q) mismatch, Shunt, Diffusion Impairment, and Hypoventilation.V/Q mismatch is the most important and common mechanism. Areas of low ventilation relative to perfusion (low V/Q units) lead to hypoxemia.Shunts can be intracardiac or intrapulmonary.
10Causes of Hypercapnic Respiratory Failure Primary Alveolar HypoventilationObesity Hypoventilation SyndromeSevere Pulmonary EdemaSevere ARDSMyxedemaTetanusCOPDStatus AsthmaticusDrug OverdosePoisoningsMyasthenia gravisGuillain-BarreHead and Cervical Cord InjuryPoliomyelitisPolyneuropathy
11SUMMARY Two types of acute respiratory failure: Type I : Hypoxemic , where PaO2 < 60 mmHgType II : Hypercapnic , where PaCO2 > 50 mmHgNB* : for status asthmaticus, PaCO2 > 40 mmHg signifies hypercapnic respiratory failure.V/Q mismatch is the most common mechanism for both types of respiratory failure.Many conditions can cause both hypoxemia and hypercapnia : e.g., COPD, Obesity, ARDS, severe pulmonary edema, neuromuscular disorders.Avoid worsening hypercapnia by judiciously giving the patient supplemental oxygen.Some patients may require NIPPV or mechanical ventilation.
14BENEFITS OF NIV Avoid complications of ETI VAPSepsis/shockTracheostomyGI bleedDVTDecrease mortality associated with respiratory failureUse NIV in the place of IMVAssist DNI patients with respiratory failureSymptomatic relief of dyspneaCorrection of gas exchangeImprove lung mechanicsFacilitate sleepCorrect mental statusPre-oxygenate for intubationPrevent ETI
15PHYSIOLOGIC MECHANSIMS Unload respiratory muscles inspiratory cycle:hyperinflation >> respiratory muscle shortening/disadvantageDecreased compliance of respiratory systemNIPPV = augments respiratory effort, Increases Vt, decreases RROvercome intrinsic peepintrinsic peep>> difficulty in generating pressure gradient for flowCPAPStent open lower airway expiratory cycleCPAP to reduce obstructionStent open upper airway
16PHYSIOLOGIC MECHANSIMS Reduce CO2 productionNIPPVImprove gas exchange by decreasing atelectasisCPAP/NIPReduce negative intra-thoracic pressure swingsCPAPRedistribute pulmonary edemaCPAP/NIPPVIncrease CO by decreasing effective LV afterload
18Contraindications for NIV Inability to protect airwayimpaired cough or swallowingpoor clearance of secretionsdepressed sensorium and lethargyStatus epilepticusPotential for upper airway obstructionExtensive head / neck tumorsAny other tumor with extrinsic airway compromiseAngioedema or anaphylaxis causing airway compromise
19Candidates for NIVPatient cooperative (excludes agitated, belligerent, comatose patients)Dyspnea (moderate to severe, short of respiratory failure / agonal breathing)Tachypnea (rr> 24 /min)Increased work of breathing (+accessory muscle use, pursed lip breathing)Hypercapnic respiratory acidosis (pH range 7.10 – 7.35)Hypoxemia (PaO2/FiO2 < 200 mm Hg, best in rapidly reversible causes for hypoxemia)
20Suitable Clinical Conditions for NIV Most patients with :COPDCardiogenic pulmonary edemaSelected patients with :CAP + COPDAsthma / CFDecompensated OSA/OHS, cor pulmonaleARDSImmunocompromised state / mild PCPNeuromuscular respiratory failureDNI +/- DNR statusPost extubation COPD / post –op respiratory failure
21NIV: utilization classification mandatory ventilationAlternative to intubationsevere ARF, meet criteria for IMVFailed medical treatmentTrials: NIV vs IMV after failed MTPrimary outcome: mortalitysupportive ventilationPrevent intubationmild-to-moderate ARF/does not meet criteriafor IMVTrials: NIV+MT vs MTPrimary outcome: intubation
22NIV: utilization classification prophylactic ventilationTo prevent ARF in patientsno substantial impairment of gas exchangeTrials: NIV+MT vs MTPrimary outcome: Blood gas values, FEV1, etcother purpose ventilationbronchodilationPre-oxygenationFacilitate sleep
23NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, SUPPORTIVE VENTILATION RCTINCLUSION CRITERIACOPD with exacerbation of dyspnea > two days and at least two of the following:RR>30PaO2 < 45 mm HgpH < 7.35 after > 10 min on RAEXCLUSION CRITERIARR< 12 breaths, sedative drugs within the previous 12 hoursCNS disorder unrelated to hypercapnic encephalopathy or hypoxemiaCardiac arrest (within the previous five days)Cardiogenic pulmonary edemaAsthma
24NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, SUPPORTIVE VENTILATION RCTkyphoscoliosis as the cause of chronic respiratory failureneuromuscular disorder as the cause of chronic respiratory failureUpper airway obstruction, facial deformity, tracheotomyneed for immediate intubation = a clear cause of decompensation requiring specific treatment (e.g., peritonitis, septic shock, AMI)pulmonary thromboembolismpneumothorax, hemoptysissevere pneumoniarecent surgery or trauma
25Primary outcome: need for intubation Secondary outcomes: LOS hosp, complications, length of MV, in hosp mortalityStandard treatment arm`O2 via NC up to 5 liters for target sat > 90%Medications: SQH, antibiotics, bronchodilators, IV corticosteroids or aminophyllineNIPPV treatment arm:same as above andBIPAP at least 6 hours/day, NC for at least 2 hours/dayIP=20, EP=0, flow cycled, PAC if patient is apneic
26Primary outcome: need for intubation Secondary outcomes: LOS hosp, complications, length of MV, in hosp mortalityMajor Criteria for intubation:respiratory arrest, pauses with LOC, gasping, requiring sedation, HR<50 with lethargy, SPB<70Minor Criteria for intubation:RR> 35 and > on admission, pH < 7.3 and < admission, PaO2<45 despite O2, worsening MSOne Major Criteria or 2 Minor Criteria after one hour of RX would be indication for intubation.In the NIPPV group if 2 minor criteria met off NIV, they can be placed back on it. But if problem persisted then intubation performed
27NIV for acute exacerbations COPD Brochard, NEJM, 1995
28Primary outcome: need for intubation 85 patients total42 standard rx (ST) group 31 intubated (74%)43 NIPPV rx group intubated (26%)ARR = 48%, NNT= 2Major criteria for intubation met by 10/31 (ST) and /11 (NIPPV)At 1 hour:NIPPV group:improved encephalopathy, rr, PaO2, pHStandard group:worsening enceph, PaCO2, pH
29Encephalopathy score1= mild asterixis,2= marked asterixis, mild confusion, sleepy during the day3= major confusion with daytime sleepiness or agitation
30Primary outcome: need for intubation Need for intubation was associated with:Higher SAP scoresHigher encephalopathy scores on admission.On admission prior to randomization:ST 1.6NIPPV 1.8At one hour:the scores worsened in ST 1.9improved in NIPPV 1.5 (and 0.8 at 12h)Results:ST group no ETI = 0.7; +ETI = 1.9NIPPV group no ETI = 1.6; +ETI = 2.5
31Success probably related to rapid improvement in encephalopathy NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, SUPPORTIVE VENTILATION RCTSuccess probably related to rapid improvement in encephalopathyMortality: ST 29% (32% intubated)NIPPV: 9% (25% intubated)Complications in ST 48%, NIPPV 16%NIPPV group: average NIPPV = 4 days; average MV = 25 daysST group: average MV =17 dLOS: ST 35 days, NIPPV 23 days
32Noninvasive positive pressure ventilation in acute respiratory failure due to COPD vs other causes: Ritesh Agarwal, Rajesh Gupta, Ashutosh N Aggarwal, Dheeraj GuptaSUPPORTIVE VENTILATION:Both hypoxic and hypercapnic patients responded to NIV:COPD patients improved their PCO2 and pHPNA/ARDS patients improved their PAO2Avoided ETI in 87% of COPD patients and 61% all other etiologiesMortality: 12% in COPD, 18% other etiologies
33Non-invasive positive pressure ventilation in acute respiratory failure due to COPD vs other causes: R Agarwal, R Gupta, A N Aggarwal, D Gupta: Supportive ventilationMIXED POPULATION STUDYPrimary outcome:NIPPV failure defined as inability to stabilize or improve in 60 mingas exchangedyspneamental status
34Noninvasive positive pressure ventilation in acute respiratory failure due to COPD vs other causes: Ritesh Agarwal, Rajesh Gupta, Ashutosh N Aggarwal, Dheeraj GuptaEtiology is the only independent predictor of outcome: STUDIES WITH MIXED POPULATIONS ARE VIRTUALLY MEANINGLESSNIPPV failure rate is very high in Pneumonia, ARDS:transient improvement in RR, HR and blood gas parameter does occurthe underlying process such as sepsis or pneumonia is not affected by NIPPVimprovement with antibiotics and other supportive measures takes at least hours which can cause late NIPPV failure despite an improvement in the first few hours
35RECOMMENDED ALGORITHM Noninvasive ventilation in acute exacerbations of COPD M.W. Elliott, Eur Respir Rev 2005
36Factors for NIV Failure NIPPV failure: likely to need intubationAPACHE 2 score higher than 29Higher PaCO2 on admission (>85)Lower pH( 7.2 or less) leads to higher intubation rates but not worse outcomesFailure to reduce PaCO2 in 1-2 hoursoften related to air leak/poor interfaceHypercapnic encephalopathyAsynchrony, copious secretionsDespite higher ETI in the likely to fail group this did not lead to higher mortality from trial of NIV
37SEVERE ACUTE ASTHMA Increased WOB secondary to inspiratory cycle: hyperinflationexpiratory cycle: airway obstructionIncreased CO2 production secondary to increased WOBDecreased CO2 eliminationMucus plugging resulting in atelectasis and hypoxemiaRational for BPAP/CPAP: unload respiratory muscles during inspiration and reduce obstruction with CPAP: airway stentingImprove gas exchange by eliminating atelectasis, distribute BD’s
38A Pilot Prospective, Randomized, Placebo-Controlled Trial of Bilevel Positive Airway Pressure in Acute Asthmatic Attack, Arie Soroksky, MD, Chest PROPHYLACTIC VentilationPatients in EDNasal BPAP at EPAP 5, IPAP 8-15pH both groups 7.4, PCO2= 34FEV137% 57% pred in NIV group34% 44% pred in controlAlso significant improvement in ED d/c rates, RR
39A Prospective RCT on the Efficacy of Noninvasive Ventilation in Severe Acute Asthma: Dheeraj Gupta MD DM, SUPPORTIVE VentilationClearly not the most severe status asthmaticus group but initial FEV1= 23% pred and RR 37, P/F ratio < 300 and normocapnea25 pt in each arm treated in a respiratory ICUDoes not show significant statistical differences in improvement of FEV1, RR, or P/F ratio between the two groups+ trend toward a quicker reversal of bronchial obstruction= 50% improvement in (FEV1) at 4 hours of treatment (64% vs 86%)
40A Prospective RCT on the Efficacy of Noninvasive Ventilation in Severe Acute Asthma: Dheeraj Gupta MD DM, SUPPORTIVE VentilationShorter ICU stay (median 10 h vs 24 h) and hospital stay (median 38 h vs 54 h)Lower doses of BD were used in NIV group4 pts in med arm had treatment failure but improved with NIV (masking potential benefit of NIV arm or need for intubation) (no one in the ST group was intubated)2 patients on NIV required IMV for respiratory fatigue, hypoxia, and agitationThere was no mortality in either group
41Noninvasive Positive Pressure Ventilation in Status Asthmaticus, Meduri, G: Chest 1996 MANDATORY VENTILATION17 patients with severe asthma exacerbation, not improved with medical management, and not immediately intubated in ED.Average pH 7.25, PCO2 672 required intubation due to rising PCO2There were no controls
42Non-invasive mechanical ventilation during status asthmaticus: M. M Non-invasive mechanical ventilation during status asthmaticus: M.M. Fernandez MANDATORY VENTILATIONRetrospective Observational Cohort StudyStatus defined as:hr > 140/min, +dyspnea, +accessory muscle use,rr >35/min, pulsus paradoxus >18 mmHg, PEF <100 l/min,hypercapnia14 medically managed patients improved and did not need MV or NIMV5/11 MV patients intubated in EDNIMV not started until patients arrived in ICU22 pts were started on NIMV (CPAP 7 and BIPAP 10/5) because their PCO2 was rising (53 63)3 were later intubated, 1/3 died of VAP, no other complications were noted
43Non-invasive mechanical ventilation during Status Asthmaticus: M. M Non-invasive mechanical ventilation during Status Asthmaticus: M.M. FernandezRR declined more slowly than in the MVboth PCO2 and RR did not improve at tx to ICU but improved rapidly after NIV initiationAll blood gases eventually normalizedP/F ratio:MV 212 improved to 285NIV 261 improved to 292Medical group 314 improved to 324Overall:some improved with med therapysevere cases required intubationmoderate cases were not harmed by NIV
44SUMMARY of RESULTS: NIV for ASTHMA Some patients need to be intubated immediately:NIV is Contraindicated:CAChemodynamic or electrical instabilitylife threatening hypoxemiaAMSSevere respiratory acidosis is a relative contraindication“Mandatory Ventilation” Has no RCT associated with it.Meduri and Fernandez retrospective studies show that a trial of NIV can correct impaired gas exchange (pH 7.2, 7.25) without increasing risk to patient.
45SUMMARY of RESULTS: NIV for ASTHMA “Supportive Ventilation” one RCTDid not show significant differences in improvement ofFEV1, RR, or P/F ratioDid show decreased ICU and hospital los, Intubation rates ? increased“Prophylactic Ventilation” one RCTSignificant differences in improvement of FEV1 and rr“Inhaler ventilation/ bronchodilator delivery”Some significant improvement in FEV1 with or without BD’s
46Non-invasive pressure support ventilation in severe CAP, Jolliet, Intensive care medicine, 2001, Observational study: SUPPORTIVE VENTILATIONOxygenation and RR improved in allDrager: PS 15/PEEP5Only 5 pts wore NIV continuouslyEffects of NIV dissipated 30m post d/cLikely effect of NIV: recruitment, reduction in dyspnea, RR, WOB, oxygen consumption, improved gas mixing on inspiration.16/24 were intubatedMortality IMV= 8/16, NIV only 0/8Difference on admission between groups only in average age ETI 55, NIV only 37COPD, APE, restrictive lung dz patients were excluded.
47NIV for PNA SUMMARY of FINDINGS 4 trials: observational, supportive RCT x 2, mandatory RCT x 1Supportive ventilation 1 RCTDecreased mortality and intubation rates for PNA + COPDIncreased mortality for non- COPD patientsSupportive ventilation 2 RCTDecreased mortality and intubation ratesDecreased HAP, septic shockSupportive ventilation 3 observationalDecreased mortality in patients not requiring intubation 0/8 vs 8/16ETI patients 16/24 were olderMandatory Ventilation8/8 patients in the NIV arm were intubatedMortality trended toward better in NIV group
48Observational case-control study of non-invasive ventilation in patients with ARDS, Domenighetti, G Mandatory Ventilation24 patients with ARDS: matched for age SAP score, P/F and pH12 placed on NIV,12 immediately ETINIV failed in 4/12 patients secondary to distant organ failures.NIV success patients had:reduced cumulative time on ventilation ; reduced los in ICUAfter the first 60h of ventilation:PaO2: NIV= 146 +/- 52 mmHg vs ETI= 109 +/- 34 mmHg; p = 0.05ICU mortality rate did not differ significantly between the groups but tended to be higher in the NIV group.
49NIV for ARDS/ALI No RCT dedicated to ARDS/ALI Other trials: Ferrer: intubation rates NIV 6/7, control 8/8mortality rates NIV 71%, control 88%Antonelli: Multicenter Survey:SAPS > 34 and P/F < 175 after 1 hour NIV associated with need for ETISameer Rana: ALI: cohort study: predictors of failureShock but not sepsis, lactic acidosisSevere hypoxemia PaO2/FiO2 < 147Higher Vt, minute ventilation causing lung injuryPatients who failed had a higher mortality than predicted by APACHE score
50Cardiogenic pulmonary edema The Rational: effects of CPAP/PSaugmentation of cardiac output and oxygen deliveryimproved functional residual capacityimproved respiratory mechanicsdecreased left ventricular afterload
51Redistribution of H2O Application of CPAP/PEEP to the edematous lung decreases intra-alveolar fluid volumemoves of water from interstitial spaces where gas exchange occurs (between the alveolar epithelium and pulmonary capillary endothelium) to the more compliant interstitial spaces (peribronchial and hilar regions)Redistribution of interstitial water improves oxygenation, lung compliance and V/Q matching.
52Increasing FRCCPAP/PEEP results in an increased FRC by two distinct mechanisms:10 cm H2 O or less increases the volume of patent alveoli10 cm H2 O or more is generally responsible for alveolar recruitment
53Effects of Nasal CPAP on Cardiac Output D M Baratz Responders vs non respondersMean PCWP 26 vs 27HR 92 vs 109, EF 30 vs 23%Non responders c/w responders had higher HR, lower EF. were more preload dependent
54Ventilatory and hemodynamic effects of CPAP in left heart failure Ventilatory and hemodynamic effects of CPAP in left heart failure. Lenique F, Habis M, Lafosa F, et al.Nine patients with acute heart failurePCWP >18, CI < 2.8CPAP pressures 5, 10Results: no change in SV or COlung compliance from 60 to 87WOB 18 j/min to 12 j/min+ reduction in LVEDPno change in CO noted
55CPAP vs. BIPAPThere appears to be trend in mortality benefit in BIPAP vs. CPAPNo difference measured in avoidance of IMVIncreased incidence of ACS may be attributable to:Lower PEEP levels used for BIPAP vs. CPAPability to reduce PaCO2 and vasoconstrict more readily with BIPAP than CPAPAsynchrony of patient with BiPAP
58Pooled treatment failure: Clinical practice guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway pressure in the acute care setting Sean P. Keenan , MD, CMAJ, 2011Pooled treatment failure:NIPPV RR 0.36, 95% CI 0.25–0.51CPAP RR 0.23, 95% CI 0.17–0.32Trend toward lower hospital mortalityNIPPV RR 0.84, 95% CI 0.63–1.13CPAP RR 0.73, 95% CI 0.51–1.05
59Treatment of patients with DNI status Two basic usesFor prolonged survival: Very effective in COPD and CPEHospital survival rates > 50%High failure rates in hypoxemic respiratory failure, post-op and end stage cancer.For palliation of dyspnea or delay of death for arrival of family memberCan be applied to any underlying diagnosisReassess that palliation has actually occurred.
60Evidence for efficacy and strength of recommendation: Noninvasive ventilation in acute respiratory failure Nicholas S. Hill, MD; John Brennan, MD; Erik Garpestad, MD; Stefano Nava, MD 2007Strength of RecommendationRecommended: first choice for ventilatory support in selected patientsGuideline: can be used in appropriate patients but careful monitoring advisedOption: suitable for a very carefully selected and monitored minority of patients.Level of evidenceA: multiple randomized controlled trials and meta-analysesB: more than one randomized, controlled trial, case control series, or cohort studiesC: case series or conflicting data