Transcript Non-Invasive Ventilation – Dr Chung

NON-INVASIVE VENTILATION IN ACUTE
RESPIRATORY FAILURE
Virginia Chung, MD
Chief, Pulmonary & Critical Care Medicine
Jacobi Medical Center
January 30, 2013
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
 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.
 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
 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.
 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.
 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.
 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)
 Hypersensitivity Pneumonitis
 Congenital Heart Disease
 Bronchiectasis
 Fat Embolism Syndrome
 Kyphoscoliosis
 Obesity
 Massive Pleural Effusions
 Pulmonary Hemorrhage

Primary Alveolar
Hypoventilation

Obesity Hypoventilation
Syndrome
 Poisonings

Severe Pulmonary Edema
 Myasthenia gravis

Severe ARDS
 Guillain-Barre

Myxedema
 Head and Cervical Cord Injury

Tetanus
 COPD
 Status Asthmaticus
 Drug Overdose
 Poliomyelitis
 Polyneuropathy
 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.
NIPPV / NIV / BPAP/ BiPAP
BiPAP Graphics
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
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
PHYSIOLOGIC MECHANSIMS
 Reduce CO2 production


Improve gas exchange by decreasing atelectasis


CPAP
Redistribute pulmonary edema


CPAP/NIP
Reduce negative intra-thoracic pressure swings


NIPPV
CPAP/NIPPV
Increase CO by decreasing effective LV afterload

CPAP
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
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
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)
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
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
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
NON-INVASIVE VENTILATION FOR ACUTE
EXACERBATIONS OF COPD
BROCHARD, MANCEBO, WYSOCKI: NEJM, 1995

SUPPORTIVE VENTILATION RCT
INCLUSION CRITERIA
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
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
Primary outcome: need for intubation
Secondary 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
Primary outcome: need for intubation
Secondary 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
NIV for acute exacerbations COPD
Brochard, NEJM, 1995
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
Encephalopathy score
1= mild asterixis,
2= marked asterixis, mild confusion, sleepy during the day
3= major confusion with daytime sleepiness or agitation
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
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:

ST group:

LOS: ST 35 days, NIPPV 23 days
average NIPPV = 4 days; average MV = 25 days
average MV =17 d
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
Non-invasive positive pressure ventilation in acute respiratory
failure due to COPD vs other causes:
R Agarwal, R Gupta, A N Aggarwal, D Gupta:
MIXED POPULATION STUDY
Primary outcome:
NIPPV failure defined as
inability to stabilize or improve
in 60 min
gas exchange
dyspnea
mental status
Supportive ventilation
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
RECOMMENDED ALGORITHM
Noninvasive ventilation in acute exacerbations of COPD
M.W. Elliott, Eur Respir Rev 2005
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
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
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
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%)
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
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
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
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
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.
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
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.
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
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.
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

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
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.
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
Effects of Nasal CPAP on Cardiac Output
D 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
 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
al.
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
Gray, NEJM, 2008
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, 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
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.
Evidence 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 2007

Strength of
Recommendation

Recommended:
first choice for
ventilatory support
in selected patients

Guideline: can be
used in appropriate
patients but careful
monitoring advised
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
Option: suitable
for a very carefully
selected and
monitored minority
of patients.