Nessun titolo diapositiva

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NIV ipossiemico
Divisione Pneumologia Riabilitativa e Centro
svezzamento Fondazione S. Maugeri IRCCS
Lumezzane (BS)
Dott Michele Vitacca
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DAY I 4.45 pmEmergency Room

• 49 year old woman, professional vocalist at the
  Scala
• BMI21
• Emergency Room for dyspnea (onset 24 hr before),
  thoracic pain and Fever
• Previous history Known to have mild emphysema
  treated with LABA and ICS. No major complains
  when she sings. No PFTs available

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DAY I 4.55 pm Emergency Room

• Kelly 1 (normal sensorium)
• Some bilateral crackles
• 24 breaths/min. No recruitment accessory muscles
• SaO2 94 with FiO2 50 (Venturi mask)
• BP 90/45 mmHg
• HR 124 b/m
• Body T. 38.8
• Waiting for chemical examinations, Chest X-ray,
  Urinary culture

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DAY I 5.15 pm Emergency Room

• ABG with a FiO2 of 50
• pH 7.37
• PaCO2 48 mmHg
• PaO2 75 mmHg
• PaO2/FiO2 150

• Hb 12.5 g/dl
• Ht 43
• WBC 27.000
• Albumin 3gr
• Cl- 110
• Na 144
• K 3.1
• Creat 1.2

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Chest X-ray
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What would you do?

1. Perform a CPAP trial in the ER
2. Transfer the patient to a protected
   environment
3. Perform a NIV trial (by Bilevel mode) in the ER

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What would you do?

1. Perform a CPAP trial in the ER
2. Transfer the patient to a protected
   environment
3. Perform a NIV trial (by Bilevel mode) in the ER

8
Definition ofACUTE RESPIRATORY FAILURE

• PaO2/FiO2 lt 300

PaO2/FiO2 ratio of 150 is a sign of SEVERE
hypoxia necessitating Intensive monitoring and
treatment
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High-Dependency Respiratory Unit
DAY I 6.30 pm

• Started therapy with
• Ciprofloxacin 500 mg x 2/die
• Clarytromycicn 500 mg x 2/die
• Methilpredisolone 40 mg/die
• Aspirin 500 mg ev

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DAY I 8.30 am

• Kelly 1
• Body T 37.9
• Respiratory rate 28 breaths/min
• Minimal recruitment of accessory muscles

11
ABG on Venturi mask 50

• pH 7.33
• PaCO2 51 mmHg
• PaO2 65 mmHG with FiO2 Venturi 50
• PaO2/FiO2 105 mmHg
• Bic 28.4
• BE 4.3

12
NIV should be started!
She has become more hypoxic and hypercapnic
13
Which mode?

1. CPAP
2. PSV extPEEP
3. PSV without extPEEP

14
Which mode?

1. CPAP
2. PSV extPEEP
3. PSV without extPEEP

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USE PSV CPAP or extPEEP!

• Greater improvement of hypoxia
• Greater reduction of diaphragmatic effort
• Greater reduction of dyspnea

-
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Which interface?

1. Nasal Mask
2. Full Face Mask
3. Helmet

17
Which interface?

1. Nasal Mask
2. Full Face Mask
3. Helmet

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DAY II 10.30 am

• NIV is started
• PSV CPAP
• ICU ventilator with leak
  compensation
• Full face mask
• Following settings
• FiO2 21
• PS 18 cmH20
• CPAP 8 cmH20 to get a
  SaO2gt88, then
• increase FiO2 to get a SaO2 gt
  93
• Final FiO2 45

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ABG 1hr after NIV

• pH 7.39
• PaCO2 31 mmHg
• PaO2 71 mmHG
• Bic 3
• BE 26.2
• SaO2 92
• PaO2/FiO2 157

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Are we happy?

• Yes because ABG 1 hr after NIV predict a good
  prognosis
• No because a PaO2/FiO2 lt 200 after 1 hr of NIV
  is associated with a higher NIV failure in ARF
• Yes, but caution should be excercised because
  the diagnosis of CAP is independently associated
  with a higher risk of NIV failure

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Are we happy?

• Yes because ABG 1 hr after NIV predict a good
  prognosis
• No because a PaO2/FiO2 lt 200 after 1 hr of NIV
  is associated with a higher NIV failure in ARF
• Yes, but caution should be excercised because
  the diagnosis of CAP is independently associated
  with a higher risk of NIV failure

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Antonelli et al.
272001 pag.1718-28
This observational study shows that the outcomes
of NIV during hypoxic RF may differ according to
the underlying pathologies. The likelihood of
failure is very low in patients affected by
Cardiogenic Pulmonary Edema but it is very high
in patients with CAP.
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DAY III. continuing story

• The patient was continuously monitored
• ABG were taken after 1hr and then every 3 hrs for
  the following 12 hrs
• She tolerated NIV well and the last ABG during
  spontaneous breathing showed
• pH 7.39
• PaCO2 37 mmHg
• PaO2 82 mmHG (with a FiO2 35)
• PaO2/FiO2235
• Respiratory rate 16 breaths/min

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Remembershe was also a COPD patient
25
Intubation
2-months mortality

26
The message to take home

• NIV used in a protected environment may PREVENT
  endotracheal intubation in HYPOXIC patients with
  pneumonia, but ONLY in those patients with
  pre-existing COPD

27
IN THE FOLLOWING DAYS.

• She improved daily and NIV was stopped on day 4,
  after having progressively reduced the duration
  of its application

28
INSUFFICIENZA RESPIRATORIA ACUTA
Depressione del Drive Respiratorio Agenti
sedativi Grave Alcalosi Metabolica Lesioni del
midollo spinale
DRIVE

• Aumento della VE
• Dolore, Ansietà
• Sepsi
• Aumento VD/VT

• Riduzione della forza
• dei muscoli respiratori
• Malnutrizione
• Iperinsufflazione Polmonare
• Miastenia Gravis
• Fattori metabolici

• Aumentato Carico
• Elastico
• Bassa Compliance polmonare
• Bassa Compliance toracica
• PEEP intrinseca

• Anomalie della parete
• toracica
• Volee costale
• Dolore post-toracotomia

• Aumentato Carico
• Resistivo
• Broncospasmo acuto
• Aumento delle secrezioni
• Ostruzione delle vie aeree superiori

CARICO
CAPACITA

• Malattie Neurologiche
• Periferiche
• Danno spina cervicale
• Lesione del nervo frenico
• Disfunzione del diaframma
• post-Intervento sulladdome
• Polineuropatia da critical illness
• Sindrome di Guillain-Barrè

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RESPIRATORY FAILURE
LUNG FAILURE
PUMP FAILURE
CENTRAL DEPRESSION FATIGUE MECHANICAL DEFECT
VENTILATORYFAILURE
GAS EXCHANGE FAILURE
HYPOXEMIA
HYPERCAPNIA
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Hypoxemic Respiratory Failure (Type 1)

• Physiologic Causes of Hypoxemia
• Low FiO2 (high altitude)
• Hypoventilation
• V/Q mismatch (low V/Q)
• Shunt (Qs/Qt)
• Diffusion abnormality
• Venous admixture ( low mixed venous oxygen)

32
The 3 major determinants of hypoxemia
1st the composition of Inspired air (gas) ?Low
FiO2
I
2nd quality and capacity of the gasexchanger ?
V/Q mismatching
PAO2 (Pb-PH2O) x 0.21-PACO2/R
PaO2
3rd the composition of Mixed venous blood ?
LowPvO2
33
Common Causes of Hypoxemic Respiratory Failure

• Pneumonia
• Cardiogenic pulmonary edema
• Acute respiratory distress syndrome
• Aspiration of gastric contents
• Multiple trauma
• Immunocompromised host with pulmonary infiltrates
• Pulmonary embolism

34
Neurological Signs and Symptoms of Hypoxia
PaO2, mmHg Signs and Symptoms of Hypoxia
30 to 50 Loss of critical judgment, confusion, delirium (resembling alcohol intoxication), tremors, asterixis
25 to 35 Somnolence, obtundation, myoclonic jerks, seizures
20 to 25 Loss of consciousness
lt 20 Death
F. Laghi and M. Tobin 2013
35
Hypocapnia is a common component of many acute
illnesses, although its importance is often
underestimated. The prevalence of hypocapnia may
be exacerbated by the belief held by some
clinicians that hypocapnia is inherently safer
than or at least preferable to hypercapnia.
36
Neurologic Effects of Hypocapnia
Systemic hypocapnia results in cerebrospinal
fluid alkalosis, which decreases cerebral blood
flow, cerebral oxygen delivery, and toa lesser
extent, cerebral blood volume. The reduction in
intracranial pressure may be life saving in
patients in whom the pressure is severely
elevated. However, hypocapnia-induced brain
ischemia may occur because of vasoconstriction
(impairing cerebral perfusion), reduced oxygen
release from hemoglobin, and increased neuronal
excitability, with the possible release of
excitotoxins such as glutamate. Over time,
cerebrospinal fluid pH and, hence, cerebral blood
flow gradually return to normal. Subsequent
normalization of the partial pressure of arterial
carbon dioxide can then result in cerebral
hyperemia, causing reperfusion injury to
previously ischemic brain regions.
37
Targets of ventilation in ARF

• improvement of oxygenation
• improvement of respiratory acidosis
• reduction of work of breathing
• improvement of cardiac performance
• reduction of patients distress
• avoid EI

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Ma funziona sul serio la NIV ?
39
Direct or indirect insult
cytokines
Vasoactive mediator
Clotting system activation
Complement system activation
Endothelial/ Epithelial leak
Micro/macro thrombi
vasoconstriction
Impaired Hypoxic pulmonary vasocostriction
Alveolar oedema
V/Q mismatch
Refractory hypoxemia
Increased Pulmonary vasculare resistances
Decrease lung compliance
40
Insufficienza respiratoria Acuta
timimg oxygenation Xray wedgeP
ALI criteria Acute onset PaO2/FiO2 300 mmhg Bilateral infiltrates 18 mmhg Or absence of left atrial hypertension
ARDS criteria Acute onset PaO2/FiO2 200 mmhg Bilateral infiltrates 18 mmhg Or absence of left atrial hypertension
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CPAP IN CPE
Pes (cmH20)
Spontaneous breathing
CPAP 15 cmH20
0
-20
Rasen et al Chest 1985 87 158-162
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CPAP Cardiovascular Effects
Positive Pressure
? ITP
? FRC
? WOB
? LVafterload ? PTM
? PaO2

• Pre-load
• ? Venous return

? Cardiac performance ? pulmonary congestion
44
the correct time to start
45
IDENTIFY PATIENTS
1. Clinical abnormalities - moderate to
severe dyspnea - RR gt 24 b/min in COPD - RR
gt 30 35 b/min in AHRF - accessory muscle
use, paradoxal breathing 2. Gas exchange
abnormalities - PaCO2 gt 45 mmHg, pH lt 7.35 -
PaO2/FiO2 lt 250 mmHg
Am J Respir Crit Care M d 2001 163 283-291
Intensive Care Medicine 2001 27 166-178
46
Difficult intubation !
Am J Respir Crit Care M d 2001 163 283-291
Intensive Care Medicine 2001 27 166-178
47
Non invasive CPAP to treat PE or CHF
48
Metanalisi
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CPAP NIV
O2 02
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CPAP NIV
O2 02
52
death EI
CPAP vs NIV
53
Non-invasive positive pressure ventilation (CPAP
or bilevel NPPV) for cardiogenic pulmonary edema
(Cochrane Review) Vital FMR. et al., 2008
hospital mortality
NIV/CPAP vs 02
54
Non-invasive positive pressure ventilation (CPAP
or bilevel NPPV) for cardiogenic pulmonary edema
(Cochrane Review) Vital FMR. et al., 2008
endotracheal intubation rate
NIV/CPAP vs 02
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The best candidate
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How can we say that CPAP and NIV are equivalent
in term of delivered pressure ?
How can we identify whether there is a subset of
patients who benefit more from NIV application
than from CPAP ?
Which patients can be successfully treated only
with standard medical therapy ?
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New Variable HYPERCAPNIA
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CPE Risk Factors for NIV Failure
Arterial pressure and hypercapnia
Masip J. ICM 2003 29 1921-8
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CPE Risk Factors for NIV Failure
Masip J. ICM 2003 29 1921-8
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New Variable ACIDOSIS
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Endotracheal intubation or Non invasive
CPAP/PPV to treat Postoperative Hypoxiemic
Respiratory Failure ?
63
Causes of Postoperative Respiratory Failure

• Intrapulmonary Causes
• Atelectasis
• Aspiration
• Pneumonia
• ARDS
• Volume overload/congestive heart failure
• Pulmonary embolism (thrombus, air, fat)
• Bronchoconstriction (Asthma/COPD)
• Pneumothorax

• Extrapulmonary Causes
• Shock
• Sepsis
• Decreased respiratory motor output
• Phrenic nerve injury
• Diaphragmatic dysfunction
• Upper airway obstruction
• Obstructive sleep apnea

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• Patients scheduled for elective major abdominal
  surgery () and general anesthesia who met a
  PaO2/FiO2 lt 300 after 1 h at 30 (Venturi mask
  ) in the recovery room.
• () Opening abdominal wall and viscera exposition
  gt 90 minutes with laparotomic or subcostal
  incision .

Helmet CPAP 10 cmH2O (104 pts)
Venturi Mask (105 pts)
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Pneumonia Plt 0.019 Infection Plt 0.029 Sepsis Plt
0.033 Re-intervention Plt 0.019
Squadrone JAMA 2005
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Endotracheal intubation or Non invasive
CPAP/PPV to treat Hypoxiemic Respiratory
Failure (Pneumonia or ARDS) ?
69
Physiologic effects of non invasive ventilation
in acute lung injury LHer E, Am J Respir Crit
Care Med 2005
Less dyspnea
Similar O2 improvement
Less WOB
Less WOB
70
Predictors of failure of noninvasive ventilation
in acute hypoxiemic patients
100
NIV Efficiency ()
50
0
ACPE
COPD
ARF
Pelosi Eur Emerg J 2000
Antonelli ICM 2001
71
PaO2lt100 O2 mask driven 10 L/min

• Non rebreather valve bag mask (15L/min O2), 27
  pts
• Pressure support ventilation by mask (FiO2 100
  Peep 5 cmH2O), 26 pts

Enanched PaO2 up to 30 min after ETI
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• HYPOXEMIC ARF (ARDS) IMMUNOCOMPETENT PATIENTS
• STUDIES RCT n
  Particularities Mask Mode SUCCESS
• Meduri Chest 1996 41
  PaO2/FiO2 110 F PS/PEEP 66
• Wysocki Chest 1995 42
  F PS/PEEP 38
• Patrick AJRCCM 1996 11
  Intubation C N PAV 73
  Antonelli NEJM 1998
  64 Intubation C F
  PS/PEEP 69
• Rocker Chest 1999 12 ALI /
  ARDS F PS/PEEP 50
• PaO2/FiO2 102
• Confalonieri 1999 56 Comm.
  PN F PS/PEEP 79 vs 50
• Delclaux JAMA 2000 123 PaO2/FiO2 ?
  300 F CPAP 66 vs 61
• Ferrer AJRCCM 2003 105 PaO2/FiO2
  102 F PS/PEEP 75 vs 48

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Acute Respiratory Failure in Patients with Severe
Community-acquired Pneumonia Confalonieri M.,
et al. 1999 1601585-1591
COPD Non COPD NIV
Standard p NIV
Standard p (n
12) (n 11) (n
16) (n 17) SUCCESS
100 45 0.005 63
53 0.73 ICU Stay (days)
0.25 2.1 7.6 2.2 0.02
2.9 1.8 4.8 1.7 0.44
Hospital Stay 14.9 3.4 22.5
3.5 0.13 17.9 2.9
15.1 2.8 0.48 Hospital Death 1
(8.3) 2 (18.2) 0.59 6
(37.5) 4 (23.5) 0.47
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• NIV / IMMUNOSUPPRESSED PATIENTS
• STUDIES R.C.T n
  Particularities Mask Mode
  SUCCESS
• Bedos 66 AIDS.
  F CPAP 66
• CCM 1999 Pneumocystis
• Confalonieri 48 AIDS. (P.tis)
  F PS/PEEP 67
• ICM 2002 intubation criteria

Antonelli 40
Solid Organ F PS/PEEP 80
JAMA 2000 Transplantation
(vs 30 )
Tognet 18
Hematological N F PS/PEEP 33
Clin I C 1994
ACV Conti
16 Hematological
N PS/PEEP 69
ICM 1998 intubation criteria
Hilbert 64 Hematological
F CPAP 25 CCM 2000
Neutropenia
Hilbert 52
Hemato-Neutropenia F PS/PEEP 54
NEJM, 2001 Drug ?Immunosup. (vs
23) AIDS
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Non invasive CPAP/PPV to treat pandemic
influenzae?
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87 patients with SARS
64 Intubated or not needing MV
23 eligible
20 Enrolled
3 excluded
6 Failure
14 Success
Therefore 12/20 (60) pts were successfully
ventilated with NIV
1 death
2 Deaths
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Oxygen is therefore contra-indicated ?
60 CM
Oxygen flow 4 L/m
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Italian Experience NIV and H1N1
Number of patients
Nicolini et al. MAS in press
85
64/337 (19) Used NIV 43/64 (67) NIV Success
67/94 (71) Used NIV 22/67 (32) NIV Success
177/489 (37) Used NIV 72/177 (41) NIV Success
60/98 (61) Used NIV 46/60 (76) NIV Success
Nicolini et al MAS
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the correct time to stop
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NIV failure associated with extremely high risk
of death
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Considera la patologia !
Carlucci A. AJRCCM 2001163874
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Carlucci A. AJRCCM 2001163874
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Only 33 NIPPV success !!
Shock, metabolic acidosis (BE lt -2.5 mEq/L), and
severe hypoxemia (PaO2/FiO2lt 150 mmHg)
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lt 150 after 1hr NPPV
94

• Failure rate 70
• Patients with shock 100
• Independent predictors of NIV failure (excluded
  patients with shock)
• Metabolic acidosis
• Severe hypoxemia

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Delayed intubation and hospital mortality

• In de novo ARF
• Longer time on NIV before ETI associated with
  decreased survival, adjusted for severity scores
  and shock
• Adj. OR 0.98, 95 CI 0.97-0.99, p0.001)

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Predictors of failure NIV for hypoxaemic
respiratory failure

• Diagnosis of ARDS or pneumonia
• SAPS 35
• Lower PaO2/FIO2 (100 or below)
• Low pH
• Age gt40 years
• Septic shock
• Multiorgan system failure
• Failure to improve PaO2/FIO2 gt146 within first
  hour

Antonelli et al. Intensive Care Med 2001 27
171828 Rana et al. Crit Care 2006 10 R79
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La vita reale
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Use of non-invasive ventilation in UK emergency
departments.Browning J, Atwood B, Gray AEmerg
Med J. 200612920-1

• 95 response rate
• 148/222 (67) use NIV on a regular basis
• 86 use NIV for CPE and 81 for COPD exacerbation
• 49/148 (33) have specific NIV protocols

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NIV use according to different pathologies
OF USE
101
Interface Facial Masks
102
HELMET MASK p
HOURS OF CONTINUOUS NIV 36 29 26 13 0.05
ETI BECAUSE OF INTOLERANCE 0 8 0.05
COMPLICATIONS RELATED TO NIV (Skin necrosis, Gastric Distension, Eye irritation) 0 14 0.002
Crit Care Med 200230602-608
103
Use of masks type in the different scenarios
Crimi et al ERJ 2008
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Rotating interface strategy
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NIV/CPAP in CPE

• Should NIV/CPAP be administered to all patients
  with CPE?
• NO
• Those with ventilatory failure
• Early use is recommended
• NO superiority for survival
• YES for physiology/patient distress
• But increased discomfort
• economic advantage,
• Patients needing intubation (plan action when
  failure)
• Which mode?
• CPAP in normocapnic and NIV in hypercapnic
  patients with cardiogenic pulmonary oedema
  improves oxygenation more rapidly than standard
  therapy
• More focus on aetiology, cardiac rhythm
• The Helmet may contribute to the application of
  NIV outside the ICU in patients who do not
  tolerate the mask

108
NON INVASIVE RESPIRATORY SUPPORT IN HYPOXIEMIC
ACUTE RESPIRATORY FAILURE ?

• High percentage of failures
• Late resolution
• Difficult invasive diagnostic procedures (BAL,
  Brush)
• Risk to delay ETI
• Take care of
• Accurate selection of the patients
• - PaO2/FiO2 gt 150 mmHg,
• - Lobar densities at chest X- Ray or CT
• - Absence of hemodynamic shock (BE gt -2.5
  mEq/L)
• Empiric Antibiotic Treatment (Protocols !)
• Non invasive fast diagnostic tests (Urinary
  antigens, etc.)
• Hemocoltures
• Dont push to hard (stop NIV if PaO2/FiO2lt 150
  at 1-2 hrs)

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Successful NIV Important factors

• More likely with a good team
• A skilled, experienced staff helps to optimize
  outcomes
• The underlying disease is an important
  determinant
• Selecting appropriate patients and monitoring
  them closely
• Severity at presentation
• Change in physiology after a short period of NIV
• If failure to ventilate or oxygenate, rapidly
  assess for reversible contributing factors
• Be prepared to intubate without undue delay
• A systematic approach to troubleshooting can help
  assure the best possible NIV outcomes

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Grazie per lattenzione