Mechanical ventilation in different diseases

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					Mechanical ventilation in
   Acute severe asthma (status asthmaticus)
   Acute respiratory distress syndrome
   Neuromuscular diseases

             Dr Arthur Chun-Wing LAU
                   Associate Consultant
 Dept of Medicine (Respiratory and Critical Care Medicine)
       and Dept of Anaesthesia (Intensive Care Unit)

                        April 2005
Acute respiratory distress syndrome
ARDS: pathophysiology
 Formation of protein-rich alveolar
  edema after damage to the integrity
  of the lung’s alveolar-capillary barrier
 Can be initiated by physical or
  chemical injury or by extensive
  activation of innate inflammatory
ARDS: radiology
CT thorax
     ARDS   Normal
Physiological derangements in
 Ventilation-perfusion mismatch
 Alveolar ventilation impairment by
  excluding oxygenation
  (Intrapulmonary shunt)
 Inactivates surfactant leading to
 Decreases lung compliance (stiff
   Most studies of ventilatory strategies for ARDS and
    acute lung injury (ALI) have shown no benefit in
    terms of mortality.
   Exceptions for so-called “lung protective strategy”
     – Amato et al 1998 (N= 53), and
     – The ARDSnet mechanical ventilation study 2000
       (N = 861)
        • better outcome in the low tidal volume (6 ml/kg
          predicted body weight) group
Tidal volume
   Important to avoid over-distension of
    alveoli in the relatively normal parts of
    – start at 6-7 ml/kg predicted BW (to maintain
      plateau pressure <30-40 cm H2O)
    – allow PCO2 to rise slowly (i.e. giving kidneys
      time to compensate for respiratory acidosis),
      aim to keep pH > 7.25 (instead of aiming for a
      target PCO2, but advisable to not to allow Pco2
      to rise above 20 kPa)
Positive end-expiratory pressure
   Optimal PEEP
    – improves gas exchange by maintaining
      alveolar patency (open lung approach)
    – reduces the FiO2 required (high oxygen
      concentrations are toxic to the lung)
   Too high PEEP will cause lung injury
    and impairs cardiac output
Total PEEP levels applied in recent studies
on protective mechanical ventilation

                            Black: study patients
                            White: control patients
PEEP: setting
   no optimal way to assess "best PEEP"
    – PEEP is added in increments of 2-5 cm until
      the "best/optimal PEEP" is obtained, choose
      the level which provides the highest static
      compliance and the lowest airway plateau
    – PEEP above lower inflection point on static P-
      V curve
   PEEP over 20 cm is rarely beneficial and
    usually results in additional pressure-
    induced lung injury
Respiratory rate
 if possible use rates <30/min to
  decrease risk of dynamic
 Rates up to 35/min were used in
  ARDSnet study

   N.B. Minute volume = RR x TV
Ventilator mode
 at equivalent inspiratory times PCV has
  the advantage of higher mean airway
  pressure compared to constant flow
  volume controlled ventilation or the
  addition of inspiratory pause
 Decelerating flow volume controlled
  ventilation has a similar airway pressure
  profile to PCV but with constant volume
 ARDSnet study used volume preset assist
High frequency oscillation
   lung inflated and kept
    open with very low tidal
    volumes should result in
    minimal shear injury
   Trend to decreased
    mortality in patients
    ventilated using high
    frequency oscillation but
    the control group received
    a relatively high tidal
    volume (~10 ml/kg)
Airway pressure release ventilation
   variation of inverse ratio ventilation
   lung volume and hence oxygenation is
    maintained by continuous positive airway
   CO2 clearance is achieved by the transient
    release of circuit pressure allowing gas to escape
    and lung volume to fall
   CPAP is then re-established to the previous level,
    allowing the entry of fresh gas into the system
    patient may breathe throughout the respiratory
    cycle also known as BIPAP
Inverse ratio ventilation (IRV)
   I:E ratio > 1 can improve oxygenation
    in patients who remain hypoxic
    despite PEEP
    – not all patients benefit from this
    – muscle relaxants often required when
      I:E ratios of > 2:1 are used
    – small risk of causing haemodynamic
Prone positioning
   routine use of prone
    positioning in all patients with
    ALI / ARDS cannot be
    currently recommended due
    to a lack of clinical data
   Indications:
     – as an adjunctive therapy to
       improve oxygenation in
       established ALI and ARDS
     – considered in patients who
       require PEEP >10 cmH2O and
       a FiO2 >0.50
 should be used early within
  36 hours of the onset of
 optimum duration unknown
Prone positioning physiological
 improvement in oxygenation has been
  reported in 58 to 100 % of patients
 Respiratory mechanics: initial decrease in
  respiratory system compliance which
  subsequently improves during the prone
  period and increases when returned to
 with more prolonged prone ventilation
  there is improvement in CO2 clearance
  which is related to improvement in
  alveolar ventilation in well-perfused areas
Prone positioning: mechanism
   The mechanism of improvement in oxygenation
    with prone positioning is multifactorial
    – less dependent atelectasis and ventilation is more
    – more effective alveolar recruitment at a lower end-
      inspiratory pressure and de-recruitment will be
      minimized at lower end-expiratory pressure
    – reduction in ventilation and perfusion mismatch and a
      reduction in intrapulmonary shunt.
    – Changes in the distribution of secretions and
      extravascular lung water
Lung recruitment manoevres
 designed to improve oxygenation
  and reduce shear injury by re-
  opening alveoli thought to reduce
  shear injury at the interface between
  collapsed and open alveoli
 N.B. there are no clinical trials
  supporting the use of recruitment
Recruitment maneuvers: methods

   incremental levels of PEEP with constant peak
    airway pressure inspiratory pressure, or
   prolonged increase in pressure (eg 40-50 cmH2O)
    either as single maneuver (lasting 40-50 secs) or
    with stepwise increase in pressure with return to
    baseline between each increase, or
   pressure control ventilation at high inspiratory
    pressures either with stepwise increases with
    return to baseline between each increase or
    single maneuver lasting 120 secs, or
   BIPAP may be useful as a recruitment maneouver
    in patients who are taking spontaneous breaths
Recruitment manoevres:
Haemodynamic consequences
 fall in cardiac output
 rise in pulmonary artery pressure
 fall in blood pressure
 transient long term significance
Lung recruitment
Tracheal gas insufflation
   an adjunctive ventilatory technique
   enhance CO2 elimination efficiency
   Method
    – During expiration, fresh gas insufflated through the TGI
      catheter washes out the CO2 that remains in the dead
      space proximal to the catheter tip
   higher flows causing a greater reduction in
   Benefit
    – less CO2 is inhaled during inspiration (enhances CO2
    – has the potential to make ventilation with a lower VT
      more efficient
Aspiration of gas from the dead
space (ASPIDS)
 a new principle
 gas rich in CO2 during late expiration
  is aspirated through a channel
  ending at the distal end of the
  tracheal tube.
 Simultaneously, fresh gas injected
  into the inspiratory line fills the
  airway down to the same site.
Extracorporeal membrane
oxygenation (ECMO)
   very expensive not
    associated with
    improved survival
Partial liquid ventilation
   involves filling the lungs with a
    fluid (perfluorocarbon, also called
    Liquivent or Perflubron) which
     –   very low surface tension, similar
         to surfactant
     –   high density, oxygen readily
         diffuses through it
     –   may have some anti-inflammatory
   The lungs are filled with the liquid,
    the patient is then ventilated with
    a conventional ventilator using a
    protective lung ventilation
   Liquid will help the transport of
    oxygen to parts of the lung that
    are flooded and filled with debris,
    help remove this debris and open
    up more alveoli improving lung
ARDSnet study: Acute Respiratory Distress Syndrome Network:
Ventilation with lower tidal volumes as compared with traditional
tidal volumes for acute lung injury and the acute respiratory distress
syndrome. New Engl J Med 2000; 342: 1301 -1308

   Randomized double blind study of traditional ventilation versus
    low tidal volume ventilation.
   861 patients with ALI or ARDS were randomised
   Traditional ventilation: tidal volume of 12 ml/kg predicted body
    weight and end-inspiratory pause pressure of 45–50 cm water
   Low volume ventilation tidal volume of 6 ml/kg predicted body
    weight and end-inspiratory pressure of 25–30 cm H2O.
   Tidal volumes were adjusted up or down in 1 ml/kg
   Plasma interleukin 6 (IL-6) was measured on day 0 and day 3 in
    204 of the first 234 patients enrolled.
   Primary outcomes:
     – death before hospital discharge and successful weaning from
     – days without ventilator use from day 1 to day 28.
   Trial stopped after enrollment of 861
    patients because mortality was lower in
    the lower tidal volume group than in
    traditional tidal volume group
    – Mortality: Low volume (LV) ventilation (31%),
      Traditional ventilation (TV) 39.8%, p = 0.007
   No of days without ventilator use during
    the first 28 days greater in LV 12+/- 11
    days vs TV 10 +/- 11 days, p<0.001
   Lung protective strategies
    –   Low tidal volume (6 ml/kg PBW)
    –   High PEEP (similar outcome for lower PEEP if small TV is used)
    –   Low plateau pressure (<30 cmH2O)
    –   Permissive hypercapnia
    –   Inverse ratio ventilation if necessary
   Adjunctive
    – Prone positioning
    – Recruitment manoevres
   Experimental
    – ECMO
    – Partial liquid ventilation
    – High frequency ventilation
Status asthmaticus
Status asthmaticus: pathophysiology

 Severe obstructive airway problem
  from bronchospasm and airway
 Presence of bronchial casts
Bronchial cast
Non invasive
 insufficient data to recommend this
  form of ventilation in acute asthma
 available data suggests that it is
  probably safe
   When to ventilate, complex decision
    which needs to be based on a
    number of factors
    – rate of deterioration
    – monitor pH and PaCO2
    – respiratory rate
    – clinical signs of exhaustion
    – likely response to treatment
Goals of mechanical ventilation
   The ideal ventilator setting is to reduce
    dynamic hyperinflation (DHI)
    – limited minute ventilation (MV), using low tidal
      volume (Vt) and respiratory rate to result in
      tolerable level of gas exchange (permissive
    – extended expiratory time (TE)
    – Aim at the lowest positive inspiratory pressure
      (PIP) and the lowest expiratory lung volume,
      avoiding intrinsic positive end expiratory
      pressure (PEEP)
Ventilator modes
   volume controlled mode: guarantees
    reproducible VT despite variations of airways
    resistance but then, the consequent rise of
    pressure must be limited
   pressure controlled mode: variations of
    resistance induce important variations of VT. A
    continuous monitoring of ventilation is always
    indicated (inspiratory and expiratory parameters
    of the ventilator, saturation, capnography,
    transcutaneous pCO2, ABG)
   Assisted and spontaneous mode are not
Neuromuscular blockade
   Indicated in patients who, in spite of
    sedation, continue to breath in a
    desynchronized manner
Initial settings

   tidal volume 6-8 ml/kg
   rate 10-14
   inspiratory flow rate 80-100 L/min (maximizing
    expiratory time)
   PEEP 0 – 3 cmH2O max
    – Controversies remain
    – high PEEP may be associated with a decrease in the
      work of breathing if the extrinsic PEEP is not higher
      than the intrinsic PEEP (< 10 cm H2O)
    respiratory rate: I:E ratio of 1:3 to 1:4
   inspiratory pause: none or minimal
Evaluation of DHI
   Elevated intrinsic PEEP
    – failure of expiratory flow curve to return to the baseline before
      next inspiration
   Elevated plateau pressure (Pplat)
    – Pplat above 30 cm H2O in adults has been correlated with
   Elevated end inspiration volume (VEI)
    – measured by disconnecting sedated and relaxed patient from
      the ventilator
    – apnea interval 20 to 30 seconds so that expiratory flow ceases
    – Total expired volume is the VEI. The difference between Vt and
      VEI is the volume of gas trapped in the lungs (VDHI)
    – VEI must be < 20 ml/kg/min to reduce volu- and barotrauma
   Baro- or volu-trauma: Pneumothoraces,
    pneumomediastinum, pnemoperitoneum,
    pulmonary interstitial emphysema
   hemodynamic
    – after intubation hypotension is linked to hyperinflation,
      hypovolemia and sedation, decreased venous return,
      tissue hypoxia, arrhythmias, oedema
   mucous plugs: atelectasis
   nosocomial infection (pneumonia, sinusitis,
   unventilable thorax
Further ways to reduce
 transitory use of a high PEEP (> 10 cm
 with 100 % oxygen, ventilation with a rate
  of 2 to 3 breaths per min for several
 acceleration of expiratory flow by
  manually compressing the rib cage, the
  patient being disconnected from ventilator
Neuromuscular disease
 Removal of secretions
 Ventilatory pump failure
 Progressive atelectasis
 Increasing oxygen requirement
 Decreasing MIP and VC
Choice of ventilatory support
   Noninvasive positive-pressure
    – If reversibility is expected over hours to
      days, e.g. mild LRTI in chronic
      neuromuscular disease as polymyositis
      or MG
    – Problem: secretion retention
   Intermittent positive pressure
    ventilation via endotracheal tube
Mode of ventilation
   Assist control or high-level pressure-support
   Decelerating ramp
   High flow early in inspiration
   Larger tidal volumes (12 – 14 ml) may be better
    tolerated and maximize stimulaton of surfatant
   PEEP: use physiological PEEP (3- 5 cm H2O)
   MV adjusted for desired pH
   Flow triggering
   Tracheostomy for failure to wean within 3 weeks
Myasthenia gravis
Myasthenia gravis
   1/20 000 adults
    - females >> males
    - peak incidence in 3rd decade in
    women, in 6th in men
    - associated with other auto-immune
    diseases, particularly other organ-
    specific auto-immune diseases
MG: clinical features
 Facial muscle weakness (drooping eyelids,
  double vision)
 Muscle weakness in the arms or legs
 Difficulty in breathing, talking, chewing or
 Fatigue brought on by repetitive motions
 Sequelae
    –   aspiration due to bulbar involvement
    –   nosocomial pneumonia
    –   Atelectasis
    –   acute respiratory failure
    –   cardiac arrest
MG: pathophysiology
   auto-immune antibodies to post-synaptic ACh
    receptor in 90% (Usually IgG), and skeletal
    muscle unable to synthesize receptors at a
    sufficiently high rate to maintain normal
    neuromuscular function
   myeloid cells within thymus have ACh receptors
    on their surface which serve as a source of
    autoantigen to trigger an immune response
    – thymic hyperplasia in 70% (tend to be younger patients)
    – thymomas in 10 – 15% (tend to be elderly)
   as disease progresses pre-synapatic receptor
    may become involved
Myathenic crisis
 Predominant problem is
  neuromuscular respiratory failure
 Incidence increases markedly with
Precipitating factors
 intercurrent infection
 Pregnancy
 drugs: antibiotics (aminoglycosides,
  polymyxins, tetracycline), anti-arrhythmics
  (quinidine, quinine, procainamide), local
  anaesthetics (procaine, lignocaine),
  muscle relaxants, analgesics (morphine,
   Intubate when VC falls below 15 ml/kg
   Aims of ventilation
    – Rest patient
    – Prevent collapse and atelectasis
    – Consider witholding anticholinergics while
      patient is intubated
    – Plasmaphoresis and/or IV Ig
    – Steroids
   Duration of mechanical ventilation is
    usually short-term unless there is infective
Gullain-Barre syndrome
Gullain-Barre: clinical features
   progressive motor weakness of > 1 limb with areflexia
   Clinical (in order of importance)
    – initial rapid progression of weakness but no further
      progression by 4 weeks
    – symmetry seldom absolute but if one limb is affected opposite
      one is likely to be affected
    – mild sensory symptoms and signs
    – facial weakness common (especially in axonal degeneration
      form) and frequently bilateral.
    – Other cranial nerves may be involved, particularly those
      innervating tongue, muscles of deglutination and extraocular
    – recovery usually start 2-4 weeks after progression stops
    – sinus tachycardia, other arrhythmias and labile BP absence of
      fever at onset of neuritic symptoms
GB: pathophysiology
   postinfectious immune-mediated disease
    – Many of the identified infectious agents are
      thought to induce antibody production against
      specific gangliosides and glycolipids, such as
      GM1 and GD1b, distributed throughout the
      myelin in the peripheral nervous system, e.g.
      Campylobacter jejuni infections
   Result: Demyelination +/- axonal
Respiratory dysfunction
   impaired expiratory effort (cough)
   weakness of tongue and retropharyngeal
    muscles causes positional airway
   inspiratory muscle weakness
   increased risk of aspiration due to
    weakness of laryngeal and glottic muscles
   ventilatory drive and CO2 response
    generally normal
Assessment of respiratory function

 respiratory dysfunction may be
  compromised before clinical signs are
  clinically obvious
 ventilatory muscle insufficiency may not
  correlate well with general
  neuromuscular examination
GB: serial assessment
   respiratory rate
   paradoxical abdominal movement
   frequent changes in breathing pattern to alternate between major
    and accessory respiratory muscles
   use of accessory muscles during quiet breathing
   cough ability
   nasal speech
   difficulty with protruding tongue and difficulty swallowing
    (indicate bulbar involvement)
   atelectasis or pulmonary infiltrates on CXR
   maximum inspiratory force
     – < 20 cm H2O associated with high risk of ventilatory insufficiency
     – FVC < 15 ml/kg associated with increased risk of ventilatory failure
     – < 10 indicative of ventilatory failure ABG: changes occur late
Respiratory management
   some evidence that early intubation and
    ventilation reduces pulmonary complications
   objective criteria for ventilation include
    – VC < 10 ml/kg and
    – maximum inspiratory force < 30 cm H2O
 Do not rely on ABGs
 May require intubation at VC <15 ml/kg due to
  inability to clear secretions decision with regard
  to tracheostomy
 Apporximately 1/3 of patients no longer need
  intubation after 2 weeks
Thank you

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