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Acute Non-Invasive Ventilation in the Acute Medical Setting

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Title: Acute Non-Invasive Ventilation in the Acute Medical Setting


1
Acute Non-Invasive Ventilationin the Acute
Medical Setting
  • CMT Regional Training Day
  • Jan 2011
  • Imogen Felton
  • SpR Respiratory Medicine

2
History The Iron LungNegative extrathoracic
pressure augmenting inspiration
  • 1928 - first iron lung
  • 1952-Danish polio outbreak positive pressure
    ventilation with an ET tube was used with fewer
    side effects

3
OBJECTIVES
  • To demonstrate knowledge of
  • The rationale for particular mode of non-invasive
    ventilation.
  • different pathophysiology patterns in respiratory
    failure
  • the indications
  • the contraindications
  • And patient selection
  • In order to optimise delivery Non Invasive
    Ventilation. In 30 minutes!

4
NIV Plan of Talk
  • Interactive Cases
  • Basics of settings and NIV plans
  • COPD and Hypercapnic Failure Evidence?
  • Cardiogenic Pulmonary Oedema Evidence?
  • Take Home Points

5
Case 1 Obstructive Airways Disease
  • 62 year old with known mod-severe COPD
  • Frequent admissions over 1yr-none to ICU
  • Productive Cough with increasing SOB
  • Ambulance called and pt arrives in Resus severely
    distressed. No decreased GCS.
  • ABG
  • pH 7.28, pCO2 9.1, pO2 58 (non-rebreathe O2 mask)
  • HCO3 29.2 BE -2 Lactate 1.9
  • NIV for this patient?

6
Case 1 COPD
  • Questions in COPD and NIV?
  • When to start?
  • What and how to give it?
  • Who will benefit?
  • Who will deteriorate?
  • What is the evidence?

7
COPD
  • First patient group in whom NIV was attempted in
    the acute setting
  • First report in the literature in COPD-1989
  • Much literature now exists-including
    wellconducted RCTs
  • COPD group has the most evidence to support its
    use in the acute setting
  • Now considered to be standard of care!

8
Joint RCP and BTS Guidance 2008
  • NIV should be considered in all patients with an
    acute exacerbation of COPD in whom a
  • respiratory acidosis (pH lt7.35 PaCO2 gt6 kPa),
    which persists despite immediate maximum standard
    medical treatment on controlled oxygen therapy
    for no more than 1 hour.
  • Lightowler et al. Non-invasive positive pressure
    ventilation to treat respiratory failure
    resulting from exacerbations of chronic
    obstructive pulmonary disease Cochrane
    systematic review and meta- analysis. BMJ
    20033261857.
  • Ram et al. Non-invasive positive pressure
    ventilation for treatment of respiratory failure
    due to exacerbations of chronic obstructive
    pulmonary disease. Cochrane Database Syst Rev
    2004.

9
Select Patient Groups - Evidence
  • NIV in Acute Hypercapnic COPD
  • Reduced mortality
  • Reduced morbidity related to endotrachealintubatio
    n
  • Reduced ICU admissions
  • Reduced hospital length of stay
  • Reduced hospitalisation and mortality at 3, 6, 9
    and 12 month follow up LONG TERM MEASURES!.

Antonelli et al. NEJM 1998339429- 435Antonelli
et al. JAMA 2000283235- 241. Hilbert et al.
NEJM 2001344481-487. Confalonieri et al.
AmJRespCritCareMed19991601585- 1591
10
NIV for acute exacerbations of chronic
obstructive pulmonary disease (AECOPD)
  • Multicenter trial
  • 85/275 pts enrolled
  • FEV1 30 predicted... similar in both groups
  • 43 pts NIV vs 42 pts standard care (std)
  • Intubation 74 (std) vs 26 (NIV)
  • Mortality 29 (std) vs 9 (NIV)
  • Complications 48 (std) vs 16 (NIV)
  • Hospital LOS (d) 35 33 (std) vs 23 17 (NIV)

Brochard et al, NEJM 1995 333 817-822
11
1 hour to consider NIV Action
Plant PK, Owen JL , Elliott MW. Early use of NIV
for acute exacerbations Of COPD on general
respiratory wards a multicentre randomised
controlled trial. Lancet 20003551931-1935 Joint
RCP and BTS Concise Guidance to Acute NIV in COPD
2008
12
Clinical Inclusion and Exclusion Criteria
  • Inclusion
  • Primary diagnosis of COPD exacerbation
  • Hypercapnic respiratory acidosis pH 7.25-7.35..
  • Able to protect airway
  • Conscious and cooperative
  • Potential for recovery to quality of life
    acceptable to the patient
  • Patients wishes considered
  • BIPAP is NOT the treatment of choice for
    patients
  • primary diagnosis is heart failure
  • or pneumonia but may be used in COPD patients
    with these complications if escalation to
    intubation and ventilation is deemed
    inappropriate.

Joint RCP and BTS Concise Guidance on Acute NIV
2008
13
Clinical Inclusion and Exclusion Criteria
  • Exclusions
  • Exclusions Cont.
  • Undrainedpneumothorax
  • Upper gastrointestinal surgery
  • Inability to protect the airway
  • Copious respiratory secretions
  • Haemodynamically unstable requiring
    inotropes/pressors (unless in a critical care
    unit)
  • Patient moribund
  • Bowel obstruction
  • Life-threatening hypoxaemia
  • Severe co-morbidity
  • Confusion/agitation/severe cognitive impairment
  • Facial burns/trauma/recent facial or upper airway
    surgery
  • Vomiting
  • Fixed upper airway obstruction

Joint RCP and BTS Concise Guidance on Acute NIV
2008
14
Exacerbation of COPD
  • In acute exacerbations of COPD - pH is the best
    marker of severity.
  • pH reflects an acute deterioration in alveolar
    ventilation compared with a chronic stable state.

15
Acute NIV Who should we treat?
  • Not all trials of BIPAP and AECOPD show reduced
    mortality, reduced intubation, reduced LOS,
    reduced complications.
  • Many trial designs show heterogeneity of
    inclusion criteria pH, location, time to
    application.

16
Acute non-invasive Ventilation in COPD-
Predictors of poor outcome
  • Low pH lt7.25
  • Pneumonia (consolidation) on CXR
  • Low body weight/Low albumin
  • Bronchiectasis (excessive secretions)
  • Poor neurological status GCS lt8
  • In the above scenarios
  • Consider intubation and mechanical ventilation
    FIRST, if patient is a suitable candidate.
  • Document escalation/intubation status.

Ambrosino et al, Thorax 199550755-757 Simonds
et al, Thorax 199550595-596
17
Case 1 COPD
  • Repeat ABG after 1 hr of Medical Rx
  • pH 7.30 pCO2 8.1 pO26.5
  • SaO2 88
  • HCO3 32 on FiO2 28
  • GCS 11/15
  • ? Commence NIV WHERE?
  • Repeat ABG after 1 hr of Medical Rx
  • pH 7.21 pCO2 11.3 pO26.2
  • SaO2 86
  • HCO3 28 on FiO2 40
  • GCS 8/15
  • ? Commence NIV WHERE?

18
Goals of BIPAP
  • Relieve symptoms
  • Reduce work of breathing
  • Improve or stabilize gas exchange
  • Within 1 hour, predictor of success
  • pCO2 reduced and pH improved.
  • Optimize patient comfort
  • Achieve pt-ventilator synchrony
  • Avoid intubation
  • Be aware that BIPAP may correct CO2 - doesnt
    treat the underlying disease!

19
Mechanisms for BIPAP Success
  • Start at EPAP 4 to max 6cm H2O
  • Offsets intrinsic PEEP resulting from expiratory
    airflow obstruction and recruits alveoli/stops
    end expiratory airway collapse.
  • i.e. Improves pO2.
  • Start at IPAP 10-12cmH2O then aim 20-22cmH2O
  • Augments tidal volume for any given respiratory
    effort
  • Leads to less mechanical disadvantage and
    decreased RR (reduced work of breathing) and
    improvements in ventilation.
  • i.e. Reduces pCO2.

20
To start
  • Explain to patient, what is going to happen and
    escalation of treatment.
  • Inform relative, staff, ICU etc.
  • Optimise mask fitting.
  • Check tubing fits into machine and there are no
    air leaks

21
Acute Non-invasive ventilation
Plant PK, Owen JL , Elliott MW. Early use of NIV
for acute exacerbations Of COPD on general
respiratory wards a multicentre randomised
controlled trial. Lancet 20003551931-1935 Joint
RCP and BTS Concise Guidance to Acute NIV in COPD
2008
22
BIPAP
  • Monitor 02 sats Titrate 02 aim 88-92 (pO2 7.5)
  • May need to ? EPAP to reduce triggering effort
    (if the ventilator triggers late increasing the
    EPAP makes it easier for the patient)
  • Increasing the EPAP may increase P02

23
Indicators of success
  • Reduced level of distress
  • Mental state improvement
  • Reduced heart rate
  • Reduced respiratory rate
  • Elimination of accessory muscle use and abdominal
    paradox

24
Markers of improvement
  • ABG at 1-2 hrs (already at therapeutic settings)
  • ? pC02
  • Improving pH
  • What next?
  • If no-longer acidotic and pCO2 normalising DO NOT
    STOP!
  • Stay on settings and repeat ABG within next
    4-6hrs.
  • Aiming first 24hrs ON then wean down time on NIV.
  • If STILL acidotic and pCO2 not reducing at
    therapeutic settings after 1-2hrs gtgtgtgt ITU if
    candidate.

25
Failure to improve
  • Deterioration consider
  • Development of a complication pneumothorax,
    sputum plugging, aspiration pneumonia.
  • Always check
  • Does mask fit ?air leak
  • Tubing connected ?air leak
  • Expiratory valve ?blocked

26
PaC02 remains elevated
  • Is the patient on too much 02?
  • Adjust Fi02 to maintain sats 85-92
  • Is there excessive leakage?
  • Check mask fits
  • If nasal mask consider chin strap or full-face
    mask.
  • Is the circuit set up properly?
  • Check connections have been made correctly
  • Check circuit for leaks

27
PaC02 remains elevated
  • Is ventilation adequate?
  • Observe chest expansion
  • Increase target pressure (or IPAP) or volume
  • Consider ? RR (to increase minute ventilation)

28
PaC02 improves, P02 remains low
  • ? Fi02
  • Consider ? EPAP.

29
Basically
  • High CO2 Reduce FiO2 ? IPAP
  • Low O2 - ? EPAP

30
Late failures
  • Pts who improve initially but then deteriorate
    after 48 hours.
  • Evidence is that they do worse if NIV is
    re-applied
  • Invasive ventilation is the better option
  • However if NIV is the ceiling then its worth a
    second try.

31
Case 2 Cardiogenic Pulmonary Oedema (LVF)
  • 52 year old with known CAD and severe LV
    dysfunction
  • Acute onset of severe SOB at 0330
  • Brought to Resus, sitting bolt upright, wheezing,
    RR 30, accessory muscle use
  • ABG
  • pH 7.24, pCO2 7.8, pO2 7.2, lactate 4.2, HCO3 18
    on non-rebreathe mask.
  • NIV?

32
Case 2 Cardiogenic Pulmonary Oedema
  • How does it work?
  • CPAP Haemodynamics
  • Reduces pre-load and afterload through positive
    intrathoracic pressure
  • Stroke volume increases
  • Heart rate decreases
  • NB Both CPAP and BIPAP can lower SBP.
  • CPAP Mechanics
  • Increases FRC
  • Recruits alveoli to decrease V/Q mismatch and
    improve physiological shunt.

Chadda K et al. Crit Care Med 2002302457-2461
33
Randomized, prospective trial of Bilevel vs CPAP
in acute pulmonaryoedema
  • 13 pts nasal CPAP vs 14 pts BiPAP
  • Conventional treatment for pulmonaryoedema
  • BiPAP improved
  • PaCO2/pH
  • HR and RR
  • Dyspnea scores
  • Both reduced intubation
  • MI 71 BiPAPvs 38 CPAP

Mehta S e al, Crit Care Med 1997 25620-628
34
BIPAP in cardiogenic pulmonaryoedema
  • Multicenter study
  • 65 pts BiPAPvs 65 pts O2 alone
  • No difference
  • Intubation
  • In-hospital mortality
  • Subgroup PaCO2 gt 6 kPa
  • Reduction in intubation
  • Improvement in HR, RR, Mean BP, Borg scale

Nava S et al. Am J RespirCrit Care Med
20031681432-1437
35
Cardiogenic Pulmonary Oedema Summary
  • NIV useful in treatment of cardiogenic pulmonary
    oedema
  • CPAP preferred modality
  • Possible increased MI rate using BiPAP
  • Likely decreases intubation rate
  • BIPAP may confer higher benefit in hypercapnic
    subset
  • Larger trials to assess mortality benefit

36
Summary
  • AECOPD 1 hour of medical Rx to consider if FOR
    intubation and remember inclusion, exclusion
    criteria and poor predictor criteria. Will they
    benefit? For ITU?
  • Importance of the 1hr ABG and then the 1-2 hr
    Trial ABG at therapeutic target. Have they
    improved enough?
  • 24 hours ON even if NOT acidotic. Your weaning
    plan!
  • BIPAP is NOT mode of support in LVF.
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