NON-INVASIVE VENTILATION IN ACUTE RESPIRATORY FAILURE - PowerPoint Presentation

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NON-INVASIVE VENTILATION IN ACUTE RESPIRATORY FAILURE

Virginia Chung, MDChief, Pulmonary & Critical Care MedicineJacobi Medical CenterJanuary 30, 2013Slide2

OUTLINEAcute respiratory failureDefinitions, Pathophysiology

NIPPV / NIV / BPAP / BiPAP vs CPAPIndications / ContraindicationsUse of NIV in: COPD, Severe Asthma, CAP, ARDS, APE/CHF, DNI/DNRSummary of RecommendationsSlide3

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.BACKGROUNDSlide4

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, PE

CLASSIFICATIONSlide5

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. CLASSIFICATIONSlide6

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

FailureSlide7

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.

PATHOPHYSIOLOGYSlide8

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

FailureSlide9

Hypersensitivity PneumonitisCongenital Heart DiseaseBronchiectasisFat Embolism Syndrome

KyphoscoliosisObesityMassive Pleural EffusionsPulmonary Hemorrhage

Causes

of

Hypoxemic Respiratory

FailureSlide10

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

TetanusSlide11

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.

SUMMARYSlide12

NIPPV / NIV / BPAP/ BiPAPSlide13

BiPAP GraphicsSlide14

BENEFITS OF NIV

Symptomatic relief of dyspneaCorrection 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 failureSlide15

PHYSIOLOGIC MECHANSIMS

Unload respiratory muscles inspiratory cycle: hyperinflation >> respiratory muscle shortening/disadvantageDecreased 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

CPAPSlide16

PHYSIOLOGIC MECHANSIMSReduce CO2 production

NIPPVImprove 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

CPAPSlide17

Contraindications for NIVAbsolute contraindications:Coma

Cardiac arrestRespiratory arrestAny condition requiring immediate intubationOther contraindications (rare exceptions)Cardiac instability (shock+need for vasopressors, ventricular dysrhythmias, complicated AMI)GI bleeding – intractable emesis, uncontrolled bleedingSlide18

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 compromiseSlide19

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)Slide20

Suitable Clinical Conditions for NIVMost patients with :COPD

Cardiogenic pulmonary edemaSelected patients with :CAP + COPDAsthma / CFDecompensated OSA/OHS, cor pulmonaleARDSImmunocompromised state / mild PCP

Neuromuscular respiratory failure

DNI +/- DNR status

Post extubation COPD / post –op respiratory failureSlide21

NIV: utilization classification

mandatory ventilationAlternative 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: intubationSlide22

NIV: utilization classificationprophylactic ventilation

To prevent ARF in patientsno substantial impairment of gas exchange

Trials: NIV+MT vs MT

Primary outcome: Blood gas values, FEV1, etc

other purpose ventilation

bronchodilation

Pre-oxygenation

Facilitate sleepSlide23

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 CRITERIASlide24

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

traumaSlide25

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/day

IP=20,

EP=0

, flow cycled, PAC if patient is apneicSlide26

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<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 performedSlide27

NIV for acute exacerbations COPD Brochard, NEJM, 1995Slide28

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, pHSlide29

Encephalopathy score

1= mild asterixis, 2= marked asterixis, mild confusion, sleepy during the day3= major confusion with daytime sleepiness or agitationSlide30

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 =

2.5Slide31

NON-INVASIVE VENTILATION FOR ACUTE EXACERBATIONS OF COPD

BROCHARD, MANCEBO, WYSOCKI: NEJM, 1995 SUPPORTIVE VENTILATION RCTSuccess 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 daysSlide32

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 etiologiesSlide33

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

P

rimary outcome:

NIPPV failure

defined

as inability to stabilize or improve in 60

min

gas

exchange

dyspnea

mental statusSlide34

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 MEANINGLESSNIPPV 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 hoursSlide35

RECOMMENDED ALGORITHMNoninvasive ventilation in acute exacerbations

of COPDM.W. Elliott, Eur Respir Rev 2005Slide36

Factors for NIV Failure

NIPPV failure: likely to need intubationAPACHE 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 NIVSlide37

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’sSlide38

A Pilot Prospective, Randomized, Placebo-Controlled Trial of Bilevel Positive Airway Pressure in Acute Asthmatic Attack,

Arie Soroksky, MD, Chest 2003 PROPHYLACTIC VentilationPatients 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, RRSlide39

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 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%)Slide40

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 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 agitation

There was no mortality in either groupSlide41

Noninvasive Positive Pressure Ventilation in Status Asthmaticus, Meduri, G:

Chest 1996MANDATORY 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 controlsSlide42

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 Slide43

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 NIVSlide44

SUMMARY of RESULTS: NIV for ASTHMA

Some patients need to be intubated immediately: NIV is Contraindicated:CAChemodynamic or electrical instabilitylife 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.Slide45

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’sSlide46

Non-invasive pressure support ventilation in severe CAP, Jolliet, Intensive care medicine, 2001, Observational study: SUPPORTIVE VENTILATION

Oxygenation and RR improved in allDrager: PS 15/PEEP5Only 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

.Slide47

NIV 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 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 groupSlide48

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.Slide49

NIV for ARDS/ALI

No RCT dedicated to ARDS/ALIOther 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 scoreSlide50

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 afterloadSlide51

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. Slide52

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 recruitmentSlide53

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 dependentSlide54

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 notedSlide55

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. CPAP

ability to reduce PaCO2 and vasoconstrict more readily with BIPAP than CPAP

Asynchrony of patient with BiPAPSlide56

Gray, NEJM, 2008Slide57
Slide58

Clinical practice guidelines for the use of noninvasivepositive-pressure ventilation and noninvasive continuous

positive airway pressure in the acute care settingSean P. Keenan , MD, CMAJ, 2011Pooled treatment failure: NIPPV RR 0.36, 95% CI 0.25–0.51

CPAP RR 0.23, 95% CI 0.17–0.32

T

rend toward lower hospital mortality

NIPPV RR 0.84, 95% CI 0.63–1.13

CPAP RR 0.73, 95% CI 0.51–1.05Slide59

Treatment of patients with DNI statusTwo basic usesFor 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 memberCan be applied to any underlying diagnosisReassess that palliation has actually occurred.Slide60

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 RecommendationRecommended: 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