Download Free Medical Non-Invasive Ventilation In Acute Respiratory Failure PowerPoint Presentation

Non-Invasive Ventilation In Acute Respiratory Failure PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "NON-INVASIVE VENTILATION IN ACUTE RESPIRATORY FAILURE" by Virginia Chung, MD.

This medical PowerPoint presentation talks about non-invasive ventilation (NIV), a type of respiratory support that delivers positive pressure ventilation to the lungs without the need for invasive procedures such as tracheal intubation. It is commonly used in the management of acute respiratory failure, which is a condition where the lungs fail to adequately oxygenate the body or eliminate carbon dioxide.

Acute respiratory failure can occur as a result of a variety of conditions, such as pneumonia, chronic obstructive pulmonary disease (COPD), congestive heart failure, and acute respiratory distress syndrome (ARDS). NIV can be used as a first-line therapy in some cases of acute respiratory failure, such as those caused by COPD exacerbation, and as a bridge to intubation in others, such as ARDS.

NIV can be delivered through various interfaces, such as nasal masks, full-face masks, and helmet interfaces. The choice of interface depends on the patients clinical condition, comfort, and tolerance. NIV is usually initiated in an intensive care unit (ICU) setting and closely monitored by trained healthcare professionals.

NIV has several potential benefits over invasive mechanical ventilation, such as lower rates of ventilator-associated pneumonia and decreased length of ICU stay. However, it is not without risks, and careful patient selection and monitoring are essential to ensure its safety and effectiveness.

Overall, NIV is a valuable tool in the management of acute respiratory failure, but its use should be individualized based on the patients clinical condition and response to therapy.

Tags : non-invasive ventilation, NIV, respiratory support, acute respiratory failure, critical care medicine, critical care medicine PowerPoint presentation

Published on : Mar 28, 2023 | Views : 1692 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

NON-INVASIVE VENTILATION IN ACUTE RESPIRATORY FAILURE Virginia Chung, MD Chief, Pulmonary & Critical Care Medicine Jacobi Medical Center
Slide 2-

OUTLINE Acute respiratory failure Definitions, Pathophysiology NIPPV / NIV / BPAP / BiPAP vs CPAP Indications / Contraindications Use of NIV in: COPD, Severe Asthma, CAP, ARDS, APE/CHF, DNI/DNR Summary of Recommendations
Slide 3-

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
Slide 4-

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 failure Can be associated with virtually all acute diseases of the lung Examples: pulmonary edema, pneumonia, ARDS, PE CLASSIFICATION
Slide 5-

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 hypercapnia Examples: opiate overdose, neuromuscular disease, status asthmaticus, severe COPD. CLASSIFICATION
Slide 6-

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
Slide 7-

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
Slide 8-

Pneumonia Cardiogenic Pulmonary Edema (CHF) Non-cardiogenic Pulmonary Edema (ARDS, seizure) Pulmonary Fibrosis (IPF, sarcoidosis) COPD / Asthma Pneumothorax Pulmonary Embolism Pulmonary Arterial Hypertension (Primary, Scleroderma) Pneumoconiosis (Coal-workers) Causes of Hypoxemic Respiratory Failure
Slide 9-

Hypersensitivity Pneumonitis Congenital Heart Disease Bronchiectasis Fat Embolism Syndrome Kyphoscoliosis Obesity Massive Pleural Effusions Pulmonary Hemorrhage Causes of Hypoxemic Respiratory Failure
Slide 10-

Causes of Hypercapnic Respiratory Failure COPD Status Asthmaticus Drug Overdose Poisonings Myasthenia gravis Guillain-Barre Head and Cervical Cord Injury Poliomyelitis Polyneuropathy Primary Alveolar Hypoventilation Obesity Hypoventilation Syndrome Severe Pulmonary Edema Severe ARDS Myxedema Tetanus
Slide 11-

Two types of acute respiratory failure: Type I : Hypoxemic , where PaO2 < 60 mmHg Type 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
Slide 12-

NIPPV / NIV / BPAP/ BiPAP
Slide 13-

BiPAP Graphics
Slide 14-

BENEFITS OF NIV Symptomatic relief of dyspnea Correction of gas exchange Improve lung mechanics Facilitate sleep Correct mental status Pre-oxygenate for intubation Prevent ETI Avoid complications of ETI VAP Sepsis/shock Tracheostomy GI bleed DVT Decrease mortality associated with respiratory failure Use NIV in the place of IMV Assist DNI patients with respiratory failure
Slide 15-

PHYSIOLOGIC MECHANSIMS Unload respiratory muscles inspiratory cycle: hyperinflation >> respiratory muscle shortening/disadvantage Decreased compliance of respiratory system NIPPV = augments respiratory effort, Increases Vt, decreases RR Overcome intrinsic peep intrinsic peep>> difficulty in generating pressure gradient for flow CPAP Stent open lower airway expiratory cycle CPAP to reduce obstruction Stent open upper airway CPAP
Slide 16-

PHYSIOLOGIC MECHANSIMS Reduce CO2 production NIPPV Improve gas exchange by decreasing atelectasis CPAP/NIP Reduce negative intra-thoracic pressure swings CPAP Redistribute pulmonary edema CPAP/NIPPV Increase CO by decreasing effective LV afterload CPAP
Slide 17-

Contraindications for NIV Absolute contraindications: Coma Cardiac arrest Respiratory arrest Any condition requiring immediate intubation Other contraindications (rare exceptions) Cardiac instability (shock+need for vasopressors, ventricular dysrhythmias, complicated AMI) GI bleeding – intractable emesis, uncontrolled bleeding
Slide 18-

Contraindications for NIV Inability to protect airway impaired cough or swallowing poor clearance of secretions depressed sensorium and lethargy Status epilepticus Potential for upper airway obstruction Extensive head / neck tumors Any other tumor with extrinsic airway compromise Angioedema or anaphylaxis causing airway compromise
Slide 19-

Candidates for NIV Patient 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)
Slide 20-

Suitable Clinical Conditions for NIV Most patients with : COPD Cardiogenic pulmonary edema Selected patients with : CAP + COPD Asthma / CF Decompensated OSA/OHS, cor pulmonale ARDS Immunocompromised state / mild PCP Neuromuscular respiratory failure DNI +/- DNR status Post extubation COPD / post –op respiratory failure
Slide 21-

NIV: utilization classification mandatory ventilation Alternative to intubation severe ARF, meet criteria for IMV Failed medical treatment Trials: NIV vs IMV after failed MT Primary outcome: mortality supportive ventilation Prevent intubation mild-to-moderate ARF/does not meet criteria for IMV Trials: NIV+MT vs MT Primary outcome: intubation
Slide 22-

NIV: utilization classification prophylactic ventilation To prevent ARF in patients no substantial impairment of gas exchange Trials: NIV+MT vs MT Primary outcome: Blood gas values, FEV1, etc other purpose ventilation bronchodilation Pre-oxygenation Facilitate sleep
Slide 23-

NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, 1995 SUPPORTIVE VENTILATION RCT COPD with exacerbation of dyspnea > two days and at least two of the following: RR>30 PaO2 < 45 mm Hg pH < 7.35 after > 10 min on RA EXCLUSION 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
Slide 24-

NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, 1995 SUPPORTIVE VENTILATION RCT kyphoscoliosis as the cause of chronic respiratory failure neuromuscular disorder as the cause of chronic respiratory failure Upper airway obstruction, facial deformity, tracheotomy need for immediate intubation = a clear cause of decompensation requiring specific treatment (e.g., peritonitis, septic shock, AMI) pulmonary thromboembolism pneumothorax, hemoptysis severe pneumonia recent surgery or trauma
Slide 25-

Primary outcome: need for intubationSecondary outcomes: LOS hosp, complications, length of MV, in hosp mortality Standard treatment arm `O2 via NC up to 5 liters for target sat > 90% Medications: SQH, antibiotics, bronchodilators, IV corticosteroids or aminophylline NIPPV treatment arm: same as above and BIPAP at least 6 hours/day, NC for at least 2 hours/day IP=20, EP=0, flow cycled, PAC if patient is apneic
Slide 26-

Primary outcome: need for intubationSecondary outcomes: LOS hosp, complications, length of MV, in hosp mortality Major Criteria for intubation: respiratory arrest, pauses with LOC, gasping, requiring sedation, HR<50 with lethargy, SPB<70 Minor Criteria for intubation: RR> 35 and > on admission, pH < 7.3 and < admission, PaO2<45 despite O2, worsening MS One 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
Slide 27-

NIV for acute exacerbations COPD Brochard, NEJM, 1995
Slide 28-

Primary outcome: need for intubation 85 patients total 42 standard rx (ST) group  31 intubated (74%) 43 NIPPV rx group  11 intubated (26%) ARR = 48%, NNT= 2 Major criteria for intubation met by 10/31 (ST) and 8/11 (NIPPV) At 1 hour: NIPPV group: improved encephalopathy, rr, PaO2, pH Standard group: worsening enceph, PaCO2, pH
Slide 29-

Encephalopathy score 1= mild asterixis, 2= marked asterixis, mild confusion, sleepy during the day 3= major confusion with daytime sleepiness or agitation
Slide 30-

Primary outcome: need for intubation Need for intubation was associated with: Higher SAP scores Higher encephalopathy scores on admission. On admission prior to randomization: ST 1.6 NIPPV 1.8 At one hour: the scores worsened in ST  1.9 improved in NIPPV  1.5 (and 0.8 at 12h) Results: ST group  no ETI = 0.7; +ETI = 1.9 NIPPV group  no ETI = 1.6; +ETI = 2.5
Slide 31-

NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD BROCHARD, MANCEBO, WYSOCKI: NEJM, 1995 SUPPORTIVE VENTILATION RCT Success probably related to rapid improvement in encephalopathy Mortality: ST 29% (32% intubated) NIPPV: 9% (25% intubated) Complications in ST 48%, NIPPV 16% NIPPV group: average NIPPV = 4 days; average MV = 25 days ST group: average MV =17 d LOS: ST 35 days, NIPPV 23 days
Slide 32-

Noninvasive positive pressure ventilation in acute respiratory failure due to COPD vs other causes:Ritesh Agarwal, Rajesh Gupta, Ashutosh N Aggarwal, Dheeraj Gupta SUPPORTIVE VENTILATION: Both hypoxic and hypercapnic patients responded to NIV: COPD patients improved their PCO2 and pH PNA/ARDS patients improved their PAO2 Avoided ETI in 87% of COPD patients and 61% all other etiologies Mortality: 12% in COPD, 18% other etiologies
Slide 33-

Non-invasive positive pressure ventilation in acute respiratory failure due to COPD vs other causes:R Agarwal, R Gupta, A N Aggarwal, D Gupta: Supportive ventilation MIXED POPULATION STUDY Primary outcome: NIPPV failure defined as inability to stabilize or improve in 60 min gas exchange dyspnea mental status
Slide 34-

Noninvasive positive pressure ventilation in acute respiratory failure due to COPD vs other causes:Ritesh Agarwal, Rajesh Gupta, Ashutosh N Aggarwal, Dheeraj Gupta Etiology is the only independent predictor of outcome: STUDIES WITH MIXED POPULATIONS ARE VIRTUALLY MEANINGLESS NIPPV failure rate is very high in Pneumonia, ARDS: transient improvement in RR, HR and blood gas parameter does occur the underlying process such as sepsis or pneumonia is not affected by NIPPV improvement with antibiotics and other supportive measures takes at least 24- 48 hours which can cause late NIPPV failure despite an improvement in the first few hours
Slide 35-

RECOMMENDED ALGORITHMNoninvasive ventilation in acute exacerbations of COPDM.W. Elliott, Eur Respir Rev 2005
Slide 36-

Factors for NIV Failure NIPPV failure: likely to need intubation APACHE 2 score higher than 29 Higher PaCO2 on admission (>85) Lower pH( 7.2 or less) leads to higher intubation rates but not worse outcomes Failure to reduce PaCO2 in 1-2 hours often related to air leak/poor interface Hypercapnic encephalopathy Asynchrony, copious secretions Despite higher ETI in the likely to fail group this did not lead to higher mortality from trial of NIV
Slide 37-

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 BD’s
Slide 38-

A Pilot Prospective, Randomized, Placebo-Controlled Trial of Bilevel Positive Airway Pressure in Acute Asthmatic Attack, Arie Soroksky, MD, Chest 2003 PROPHYLACTIC Ventilation Patients in ED Nasal BPAP at EPAP 5, IPAP 8-15 pH both groups 7.4, PCO2= 34 FEV1 37%  57% pred in NIV group 34%  44% pred in control Also significant improvement in ED d/c rates, RR
Slide 39-

A Prospective RCT on the Efficacy of Noninvasive Ventilation in Severe Acute Asthma: Dheeraj Gupta MD DM, 2010 SUPPORTIVE Ventilation Clearly not the most severe status asthmaticus group but initial FEV1= 23% pred and RR 37, P/F ratio < 300 and normocapnea 25 pt in each arm treated in a respiratory ICU Does 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%)
Slide 40-

A Prospective RCT on the Efficacy of Noninvasive Ventilation in Severe Acute Asthma: Dheeraj Gupta MD DM, 2010 SUPPORTIVE Ventilation Shorter 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 group 4 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 agitation There was no mortality in either group
Slide 41-

Noninvasive Positive Pressure Ventilation in Status Asthmaticus, Meduri, G: Chest 1996 MANDATORY VENTILATION 17 patients with severe asthma exacerbation, not improved with medical management, and not immediately intubated in ED. Average pH 7.25, PCO2 67 2 required intubation due to rising PCO2 There were no controls
Slide 42-

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 <100 l/min, hypercapnia 14 medically managed patients improved and did not need MV or NIMV 5/11 MV patients intubated in ED NIMV not started until patients arrived in ICU 22 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
Slide 43-

Non-invasive mechanical ventilation during Status Asthmaticus: M.M. Fernandez RR declined more slowly than in the MV both PCO2 and RR did not improve at tx to ICU but improved rapidly after NIV initiation All blood gases eventually normalized P/F ratio: MV 212 improved to 285 NIV 261 improved to 292 Medical group 314 improved to 324 Overall: some improved with med therapy severe cases required intubation moderate cases were not harmed by NIV
Slide 44-

SUMMARY of RESULTS: NIV for ASTHMA Some patients need to be intubated immediately: NIV is Contraindicated: CAC hemodynamic or electrical instability life threatening hypoxemia AMS Severe 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.
Slide 45-

SUMMARY of RESULTS: NIV for ASTHMA “Supportive Ventilation” one RCT Did not show significant differences in improvement of FEV1, RR, or P/F ratio Did show decreased ICU and hospital los, Intubation rates ? increased “Prophylactic Ventilation” one RCT Significant differences in improvement of FEV1 and rr “Inhaler ventilation/ bronchodilator delivery” Some significant improvement in FEV1 with or without BD’s
Slide 46-

Non-invasive pressure support ventilation in severe CAP, Jolliet, Intensive care medicine, 2001, Observational study: SUPPORTIVE VENTILATION Oxygenation and RR improved in all Drager: PS 15/PEEP5 Only 5 pts wore NIV continuously Effects of NIV dissipated 30m post d/c Likely effect of NIV: recruitment, reduction in dyspnea, RR, WOB, oxygen consumption, improved gas mixing on inspiration. 16/24 were intubated Mortality IMV= 8/16, NIV only 0/8 Difference on admission between groups only in average age ETI 55, NIV only 37 COPD, APE, restrictive lung dz patients were excluded.
Slide 47-

NIV for PNA SUMMARY of FINDINGS 4 trials: observational, supportive RCT x 2, mandatory RCT x 1 Supportive ventilation 1 RCT Decreased mortality and intubation rates for PNA + COPD Increased mortality for non- COPD patients Supportive ventilation 2 RCT Decreased mortality and intubation rates Decreased HAP, septic shock Supportive ventilation 3 observational Decreased mortality in patients not requiring intubation 0/8 vs 8/16 ETI patients 16/24 were older Mandatory Ventilation 8/8 patients in the NIV arm were intubated Mortality trended toward better in NIV group
Slide 48-

Observational case-control study of non-invasive ventilation in patients with ARDS, Domenighetti, G Mandatory Ventilation 24 patients with ARDS: matched for age SAP score, P/F and pH 12 placed on NIV, 12 immediately ETI NIV failed in 4/12 patients secondary to distant organ failures. NIV success patients had: reduced cumulative time on ventilation ; reduced los in ICU After the first 60h of ventilation: PaO2: NIV= 146 +/- 52 mmHg vs ETI= 109 +/- 34 mmHg; p = 0.05 ICU mortality rate did not differ significantly between the groups but tended to be higher in the NIV group.
Slide 49-

NIV for ARDS/ALI No RCT dedicated to ARDS/ALI Other trials: Ferrer: intubation rates NIV 6/7, control 8/8 mortality rates NIV 71%, control 88% Antonelli: Multicenter Survey: SAPS > 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
Slide 50-

Cardiogenic pulmonary edema The Rational: effects of CPAP/PS augmentation of cardiac output and oxygen delivery improved functional residual capacity improved respiratory mechanics decreased left ventricular afterload
Slide 51-

Redistribution of H2O Application of CPAP/PEEP to the edematous lung decreases intra-alveolar fluid volume moves 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.
Slide 52-

Increasing FRC CPAP/PEEP results in an increased FRC by two distinct mechanisms: 10 cm H2 O or less increases the volume of patent alveoli 10 cm H2 O or more is generally responsible for alveolar recruitment
Slide 53-

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
Slide 54-

Ventilatory and hemodynamic effects of CPAP in left heart failure. Lenique F, Habis M, Lafosa F, et al. Nine patients with acute heart failure PCWP >18, CI < 2.8 CPAP pressures 5, 10 Results: no change in SV or CO lung compliance from 60 to 87 WOB 18 j/min to 12 j/min + reduction in LVEDP no change in CO noted
Slide 55-

CPAP vs. BIPAP There appears to be trend in mortality benefit in BIPAP vs. CPAP No difference measured in avoidance of IMV Increased incidence of ACS may be attributable to: Lower PEEP levels used for BIPAP vs. CPAP ability to reduce PaCO2 and vasoconstrict more readily with BIPAP than CPAP Asynchrony of patient with BiPAP
Slide 56-

Gray, NEJM, 2008
Slide 57-

ppt slide no 57 content not found
Slide 58-

Clinical practice guidelines for the use of noninvasivepositive-pressure ventilation and noninvasive continuouspositive airway pressure in the acute care settingSean P. Keenan , MD, CMAJ, 2011 Pooled treatment failure: NIPPV RR 0.36, 95% CI 0.25–0.51 CPAP RR 0.23, 95% CI 0.17–0.32 Trend toward lower hospital mortality NIPPV RR 0.84, 95% CI 0.63–1.13 CPAP RR 0.73, 95% CI 0.51–1.05
Slide 59-

Treatment of patients with DNI status Two basic uses For prolonged survival: Very effective in COPD and CPE Hospital 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 member Can be applied to any underlying diagnosis Reassess that palliation has actually occurred.
Slide 60-

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 2007 Strength of Recommendation Recommended: first choice for ventilatory support in selected patients Guideline: can be used in appropriate patients but careful monitoring advised Option: suitable for a very carefully selected and monitored minority of patients. Level of evidence A: multiple randomized controlled trials and meta-analyses B: more than one randomized, controlled trial, case control series, or cohort studies C: case series or conflicting data