PowerPoint Presentation

NON-INVASIVE VENTILATION IN ACUTE RESPIRATORY FAILUREVirginia Chung, MDChief, Pulmonary & Critical Care MedicineJacobi Medical CenterJanuary 30, 2013

OUTLINEAcute respiratory failureDefinitions, PathophysiologyNIPPV / NIV / BPAP / BiPAP vs CPAPIndications / ContraindicationsUse of NIV in: COPD, Severe Asthma, CAP, ARDS, APE/CHF, DNI/DNRSummary of Recommendations

Respiratory 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.BACKGROUND

Respiratory 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, PECLASSIFICATION

TYPE 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. CLASSIFICATION

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. Acute vs. Chronic Hypercapnic Respiratory Failure

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.

PATHOPHYSIOLOGY

PneumoniaCardiogenic Pulmonary Edema (CHF)Non-cardiogenic Pulmonary Edema (ARDS, seizure)Pulmonary Fibrosis (IPF, sarcoidosis)COPD / AsthmaPneumothoraxPulmonary EmbolismPulmonary Arterial Hypertension (Primary, Scleroderma)Pneumoconiosis (Coal-workers) Causes of Hypoxemic Respiratory Failure

Hypersensitivity PneumonitisCongenital Heart DiseaseBronchiectasisFat Embolism SyndromeKyphoscoliosisObesityMassive Pleural EffusionsPulmonary Hemorrhage Causes of Hypoxemic Respiratory Failure

Causes of Hypercapnic Respiratory FailureCOPDStatus AsthmaticusDrug OverdosePoisoningsMyasthenia gravisGuillain-BarreHead and Cervical Cord InjuryPoliomyelitisPolyneuropathyPrimary Alveolar HypoventilationObesity Hypoventilation SyndromeSevere Pulmonary EdemaSevere ARDSMyxedemaTetanus

Two types of acute respiratory failure:Type I : Hypoxemic , where PaO2 < 60 mmHgType II : Hypercapnic , where PaCO2 > 50 mmHg NB* : 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. SUMMARY

NIPPV / NIV / BPAP/ BiPAP

BiPAP Graphics

BENEFITS OF NIVSymptomatic relief of dyspneaCorrection of gas exchangeImprove lung mechanicsFacilitate sleepCorrect mental statusPre-oxygenate for intubationPrevent ETI Avoid complications of ETIVAPSepsis/shockTracheostomyGI bleedDVTDecrease mortality associated with respiratory failureUse NIV in the place of IMVAssist DNI patients with respiratory failure

PHYSIOLOGIC MECHANSIMSUnload respiratory muscles inspiratory cycle: hyperinflation >> respiratory muscle shortening/disadvantageDecreased compliance of respiratory systemNIPPV = augments respiratory effort, Increases Vt, decreases RR Overcome intrinsic peep intrinsic peep>> difficulty in generating pressure gradient for flowCPAPStent open lower airway expiratory cycleCPAP to reduce obstructionStent open upper airway CPAP

PHYSIOLOGIC MECHANSIMSReduce CO2 production NIPPVImprove gas exchange by decreasing atelectasis CPAP/NIPReduce negative intra-thoracic pressure swings CPAPRedistribute pulmonary edema CPAP/NIPPVIncrease CO by decreasing effective LV afterload CPAP

Contraindications for NIVAbsolute contraindications:ComaCardiac arrestRespiratory arrestAny condition requiring immediate intubationOther contraindications (rare exceptions)Cardiac instability (shock+need for vasopressors, ventricular dysrhythmias, complicated AMI)GI bleeding intractable emesis, uncontrolled bleeding

Contraindications for NIVInability to protect airway impaired cough or swallowing poor 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

Candidates 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)

Suitable Clinical Conditions for NIVMost 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

NIV: utilization classificationmandatory ventilationAlternative to intubationsevere ARF, meet criteria for IMVFailed medical treatment Trials: NIV vs IMV after failed MTPrimary outcome: mortalitysupportive ventilationPrevent intubationmild-to-moderate ARF/does not meet criteria for IMVTrials: NIV+MT vs MTPrimary outcome: intubation

NIV: utilization classificationprophylactic ventilationTo prevent ARF in patientsno substantial impairment of gas exchangeTrials: NIV+MT vs MTPrimary outcome: Blood gas values, FEV1, etcother purpose ventilationbronchodilationPre-oxygenationFacilitate sleep

NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, 1995 SUPPORTIVE VENTILATION RCTCOPD 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 CRITERIA RR< 12 breaths, sedative drugs within the previous 12 hours CNS disorder unrelated to hypercapnic encephalopathy or hypoxemia Cardiac arrest (within the previous five days) Cardiogenic pulmonary edema Asthma

INCLUSION CRITERIA

23NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, 1995 SUPPORTIVE VENTILATION RCTkyphoscoliosis as the cause of chronic respiratory failureneuromuscular disorder as the cause of chronic respiratory failureUpper airway obstruction, facial deformity, tracheotomy need for immediate intubation = a clear cause of decompensation requiring specific treatment (e.g., peritonitis, septic shock, AMI)pulmonary thromboembolismpneumothorax, hemoptysissevere pneumoniarecent surgery or trauma

Primary outcome: need for intubationSecondary 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 and BIPAP at least 6 hours/day, NC for at least 2 hours/dayIP=20, EP=0, flow cycled, PAC if patient is apneic

Primary outcome: need for intubationSecondary outcomes: LOS hosp, complications, length of MV, in hosp mortalityMajor Criteria for intubation: respiratory arrest, pauses with LOC, gasping, requiring sedation, HR on admission, pH < 7.3 and < admission, PaO285)Lower pH( 7.2 or less) leads to higher intubation rates but not worse outcomes

Failure to reduce PaCO2 in 1-2 hoursoften related to air leak/poor interfaceHypercapnic encephalopathyAsynchrony, copious secretions

Despite higher ETI in the likely to fail group this did not lead to higher mortality from trial of NIV

SEVERE ACUTE ASTHMA Increased WOB secondary to inspiratory cycle: hyperinflation expiratory cycle: airway obstruction Increased CO2 production secondary to increased WOB Decreased CO2 elimination Mucus plugging resulting in atelectasis and hypoxemia Rational for BPAP/CPAP: unload respiratory muscles during inspiration and reduce obstruction with CPAP: airway stenting Improve gas exchange by eliminating atelectasis, distribute BDs

A Pilot Prospective, Randomized, Placebo-Controlled Trial of Bilevel Positive Airway Pressure in Acute Asthmatic Attack, Arie Soroksky, MD, Chest 2003 PROPHYLACTIC VentilationPatients in EDNasal BPAP at EPAP 5, IPAP 8-15pH both groups 7.4, PCO2= 34FEV1 37% 57% pred in NIV group34% 44% pred in controlAlso significant improvement in ED d/c rates, RR

A Prospective RCT on the Efficacy of Noninvasive Ventilation in Severe Acute Asthma: Dheeraj Gupta MD DM, 2010 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%)

A Prospective RCT on the Efficacy of Noninvasive Ventilation in Severe Acute Asthma: Dheeraj Gupta MD DM, 2010 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

Noninvasive Positive Pressure Ventilation in Status Asthmaticus, Meduri, G: Chest 1996MANDATORY 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

Non-invasive mechanical ventilation during status asthmaticus: M.M. Fernandez 2001 MANDATORY VENTILATION

Retrospective Observational Cohort Study Status defined as: hr > 140/min, +dyspnea, +accessory muscle use, rr >35/min, pulsus paradoxus >18 mmHg, PEF 34 and P/F < 175 after 1 hour NIV associated with need for ETI Sameer Rana: ALI: cohort study: predictors of failure Shock but not sepsis, lactic acidosis Severe hypoxemia PaO2/FiO2 < 147 Higher Vt, minute ventilation causing lung injury Patients who failed had a higher mortality than predicted by APACHE score

Cardiogenic pulmonary edema The Rational: effects of CPAP/PSaugmentation of cardiac output and oxygen deliveryimproved functional residual capacityimproved respiratory mechanicsdecreased left ventricular afterload

Redistribution 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.

Increasing 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

Effects of Nasal CPAP on Cardiac OutputD M Baratz Responders vs non responders Mean PCWP 26 vs 27 HR 92 vs 109, EF 30 vs 23% Non responders c/w responders had higher HR, lower EF. were more preload dependent

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, 10 Results: 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

CPAP vs. BIPAPThere appears to be trend in mortality benefit in BIPAP vs. CPAP No 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

Gray, NEJM, 2008

Clinical practice guidelines for the use of noninvasivepositive-pressure ventilation and noninvasive continuouspositive airway pressure in the acute care settingSean P. Keenan , MD, CMAJ, 2011Pooled treatment failure: NIPPV RR 0.36, 95% CI 0.250.51CPAP RR 0.23, 95% CI 0.170.32Trend toward lower hospital mortality NIPPV RR 0.84, 95% CI 0.631.13CPAP RR 0.73, 95% CI 0.511.05

Treatment of patients with DNI statusTwo 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.

Evidence for efficacy and strength of recommendation: Noninvasive ventilation in acute respiratory failureNicholas 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 advised Option: suitable for a very carefully selected and monitored minority of patients.

Level of evidenceA: multiple randomized controlled trials and meta-analyses B: more than one randomized, controlled trial, case control series, or cohort studiesC: case series or conflicting data