Ventilatory support - Indications

Acute ventilatory insufficiency

Defined by an acute rise in PaCO2 and respiratory
acidosis (pH<7.2). PaCO2 is directly proportional to the
body‘s CO2 production and inversely proportional to
alveolar ventilation (minute ventilation minus dead
space ventilation).
May be caused by :
 Respiratory centre depression, e.g. by depressant drugs
or intracranial pathology
 Peripheral neuromuscular disease, e.g. Guillain – Barre’
syndrome, myasthenia gravis or spinal cord pathology
 Therapeutic muscle paralysis, e.g. as part of balanced
anaesthesia, tetanus or status epilepticus

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 Loss of chest wall integrity, e.g. chest trauma,
diaphragmatic rupture
 High CO2 production, e.g. burns, sepsis or severe
agitation
 Reduced alveolar ventilation, e.g. airways obstruction
(asthma, acute bronchitis, foreign body), atelectasis,
pneumonia, pulmonary oedema (ARDS, cardiac failure),
pleural pathology, fibrotic lung disease, obesity.
 Pulmonary vascular disease (pulmonary embolus, cardiac
failure, ARDS)

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 Oxygenation failure

Hypoxaemia is defined by PaO2<11kPa on

fIO2>0.4.
May be due to :
 Ventilation / perfusion mismatching (reduced ventilation
in or preferential perfusion of some lung areas), e.g.
penumonia, pulmonary oedema, pulmonary vascular
disease, extremely high cardiac output
 Shunt (normal perfusion but absent ventilation in some
lung zones) e.g. pneumonia, pulmonary oedema
 Diffusion limitation (reduced alveolar surface area with
normal ventilation), e.g. emphysema; reduced inspired
oxygen tension, e.g. altitude, suffocation
 Acute ventilatory insufficiency (as above)

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 To reduce intracranial pressure

Reduction of PaCO2 to approximately 4kPa causes

cerebral vasoconstriction and therefore reduces

intracranial pressure after brain injury. Recent studies

suggest this effect is transient and may impair an

already critical cerebral blood flow.

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 To reduce work of breathing

Controlled ventilation + sedation and muscle relaxation

reduces respiratory muscle activity and therefore work of

breathing. In cardiac failure or non-cardiogenic

pulmonary oedema the resulting reduction in myocardial

oxygen demand is easier matched to oxygen supply.

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 Indications for ventilatory support

Ventilatory support should be considered if :

 Respiratory rate > 30/min

 Vital capacity <10-15ml/min
 PaO2 <11kPa on FIO2 > 0.4
 PaCO2 high with repiratory acidosis (pH<7.2)
 VD/VT >60%
 QS/QT >15-20%
 Exhaustion
 Confusion
 Severe shock
 Severe LVF
 Raised ICP
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 IPPV – description of ventilators

Classification of mechanical ventilators

 Mechanical ventilators may be classified according to the
method of cycling from inspiration to expiration.
 This may be when a pre-set time has elapsed (time-
cycled), when a pre set pressure has been reached
(pressure-cycled) or when a pre-set volume has been
delivered (volume-cycled).
 Although the method of cycling is classified according to
a single constant, modern ventilators allow a greater
degree of control.
 In volume cycled mode with pressure limit the upper
pressure alarm limit is set or the maximum inspiratory
pressure is controlled.

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 The ventilator delivers a pre-set tidal volume ( VT) unless
lungs are non complaint or airway resistance is high.
 This is useful to avoid high peak airway pressures.
 In volume cycled mode with time limit inspiratory flow is
reduced; the ventilator delivers the pre-set VT unless
impossible at the set respiratory rate.
 If pressure limitation is unless impossible at the set
respiratory rate.
 If pressure limitation is not available this is useful to limit
peak airway pressure.
 In time cycled mode with pressure control, pre-set
pressure is delivered throughout inspirtion (unlike
pressure-cycled ventilation), cycling being determined by
time.
 VT is dependent on respiratory compliance and airway
resistance and high peak airway pressures can be
avoided. 8
 Setting up the mechanical ventilator

Tidal volume
 Normally 7-10ml/kg but may require 10-12ml/kg in acute
respiratory failure. In Severe airflow limitation (i.g.
asthma, acute bronchits) smaller VT and minute volume
may be needed to allow prolonged expiration.
Respiratory rate
 Usually set in accordance with VT to provide minute
ventilation of 85-100ml/kg/min. In time cycled or time
limited modes the set respiratory rate determines the
timing of ventilator cycles.

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Inspiratory flow
 Usually set between 40-80L/min. A higher flow rate is
more comfortable for alert patients and also allows for
longer expiration in patients with severe airflow
limitation.
 However, it is also associated with higher peak airway
pressures. In addition, the flow pattern may be adjusted
on most ventilators.
 A square wave is common but decelerating flow, by
reducing the average flow rate at a set peak flow rate,
may reduce peak airways pressure.

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I.E ratio
 A function of respiratory rate, VT, inspiratory flow and inspiratory
time.
 Prolonged expiration is useful in severe airflow limitation and a
prolonged inspiratory time is used in ARDS to allow slow reacting
alveoli time to fill.
 Alert patients are more comfortable with shorter inspiratory times
and high inspiratory flow rates.
FIO2
 Set according to arterial blood gases.
 Usual to start at FIO2=0.6-1.
Airway pressure
 In pressure controlled or pressure limited modes the peak airway
pressure (circuit rather than alveolar pressure) can be set (usually
<40 cm H2O). PEEP can be used to maintain FRC when respiratory
compliance is low.
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 Initial ventilator set-up

 Check for leaks

 Check oxygen on
 FIO2 0.6-1
 VT 7-12ml/kg
 Rate 10-15/min
 I:E ratio 1:2
 Peak Pressure <40cm H2O
 PEEP 0-5cm H2O

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 Ventilator adjustments in response to blood gas
measurements
 Low PaO2
 Increase FIO2
 Increase PEEP (may increase peak airways pressure or reduce CO)
 Increase I:E ratio
 Review VT and respiratory rate
 Consider CMV, increased sedation + muscle relaxants

 High PaO2
 Decrease PEEP (usually to 5cm H2O before reducing FIO2) Decrease FIO 2
 Decrease I:E ratio

 High PaCO2
 Increase VT (if peak airway pressure will allow)
 Increase respiratory rate
 Consider reducing respiratory rate if to high (to reduce intrinsic PEEP)
 Consider reducing dead space
 Consider CMV, increased sedation + muscle relaxants
 Consider tolerating (Permissive hypercapnia)

 Low PaCO2
 Decrease respiratory rate (to 10-12/min)
 Decrease VT (to <7ml/kg)
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 IPPV – modes of ventilation

Controlled mechanical ventilation (CMV)

 A per-set number of breaths are delivered to supply all
the patient’s ventilatory requirements. These breaths
may be at a pre-set VT (volume controlled) or at a pre-
set inspiratory pressure (pressure controlled)
Assist – control mechanical ventilation (ACMV)
 Patients can trigger the ventilator to determine the
reparatory rate but, as with CMV, a pre-set number of
breaths are delivered if the spontaneous respiratory rate
falls below the pre-set level.

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Intermittent mandatory ventilation (IMV)
 A pre-set mandatory rate is set but patients are free to
breathe spontaneously between set ventilator breaths.
 Mandatory breaths may be synchronized with a patient’s
spontaneous efforts (SIMV) to avoid mandatory breaths
occurring during a spontaneous breath.
 This effect, known as ‘stacking’ may lead to excessive
tidal volumes, high airway pressure, incomplete
exhalation and air trapping.
 Pressure support may be added to spontaneous breaths
to overcome the work of breathing associated with
opening the ventilator demand valve.

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Pressure support ventilation (PSV)
 A pre-set inspiratory pressure is added to the ventilator
circuit during inspiration in spontaneously breathing
patients. The pre-set pressure should be adjusted to
ensure adequate VT.
Choosing the appropriate mode
 Pressure controlled ventilation avoids the dangers
associated with high peak airway pressures, although it
may result in marked changes in VT if compliance alters.
 Allowing the patient to make some spontaneous
respiratory effort may reduce sedation requirements, re-
train respiratory muscles and reduce mean airway
pressures.

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Apnoeic patient
 Use of IMV or ACMV in patients who are totally apnoeic provides the
total minute volume requirement if the pre-set rate is high enough
(this is effectively CMV) but allows spontaneous respiratory effort on
recovery.
Patient taking limited spontaneous breaths
 A guaranteed minimum minute volume is assured with both ACMV
and IMV depending on the pre-set rate.
 The work of spontaneous breathing is reduced by supplying the pre-
set VT for spontaneously triggered breaths with ACMV, or by adding
pressure support to spontaneous breaths with IMV.
 With ACMV the spontaneous tidal volume is guaranteed whereas
with IMV and pressure support is that gradual reduction of pre-set
rate, as spontaneous effort increases, allows a smooth transition to
pressure support ventilation.
 Subsequent weaning is by reduction of pressure support level.

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 IPPV – failure to tolerate ventilation

 Agitation or fighting the ventilator’ may occur at any

time.
Poor tolerance during initial phase of ventilation
 Immediately after initiating mechanical ventilation the
most likely cause is a failure to match ventilator setting
to the patient’s requirements.
 Careful adjustment of VT, respiratory rate, inspiratory
flow and trigger sensitivity may resolve the problem;
alternatively, additional sedation + muscle relaxation
may be required.

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 Poor tolerance after previous good tolerance

 If agitation occurs in a patient who has previously

tolerated mechanical ventilation, either the patient’s
condition has deteriorated (e.g. tension pneumothorax)
or there is a problem in the ventilator circuit (including
artificial airway) or the ventilator itself.
 The patient should be removed from the ventilator and
placed on manual ventilation while the problem is
resolved. Resorting to increased sedation + muscle
relaxation in this circumstance is dangerous until the
cause is resolved.
 Check patency of the endotracheal tube (e.g. with a
suction catheter) and re-intubate if in doubt.
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 Consider malposition of the endotracheal tube (e.g. cuff
above vocal cords, tube tip at carina, tube in main
bronchus)
 Where patients are making spontaneous respiratory efforts
it is often better to allow this with IMV and pressure
support or, if ventilatory drive is adequate, with PSV alone,
rather than increasing sedation.
 If patients fail to sychronise with IMV by stacking
spontaneous and mandatory breaths, increasing pressure
support and reducing mandatory rate may help;
alternatively, the use of PSV may be appropriate.

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 IPPV – Complications of ventilation
Haemodynamic complications
 Venous return is dependent on passive flow from central veins to
right atrium.
 As right atrial pressure increases secondary to the transmitted
increase in intrathoracic pressure across complaint lungs there is a
reduction in venous return.
 This is less of a problem if lungs are stiff (e.g ARDS) although will
be exacerbated by the use of inverse I:E ratio.
 As lung volume is increased by IPPV the pulmonary vasculature is
constricted, thus increasing pulmonary vascular resistance.
 This increases the diastolic volume of the right ventricle and, by
sepal shift, impedes filling of the left ventricle.
 These effects all contribute to a reduced stroke volume. This
reduction can be minimized by reducing airway pressures, avoiding
prolonged inspiratory times and maintaining blood volume.
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 Ventilator trauma
 The term barotrauma relates to gas escape into cavities and
interstitial tissues occurring during IPPV.
 The complication is a misnomer since it is probably the
distending volume which is responsible rather than the
pressure. It is most likely to occur with high VT and high PEEP.
 It also occurs in IPPV and conditions associated with over
inflation of the lungs (e.g. asthma).
 Tension pneumothorax is life threatening and should be
suspected in any patient on IPPV who becomes suddenly
agitated, tachycardic, hypotensive or exhibits sudden
deterioration in their blood gases.
 An immediate chest drainage tube should be inserted if tension
pneumothorax develops. Prevention of ventilator trauma relies
on avoidance of high VT, high PEEP and high airway pressures.

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 Nosocomial infection

 Endotracheal intubations bypasses normal defence

mechanisms.
 Ciliary activity and cellular morphology in the
tracheobronchial tree are altered.
 The requirement for endotracheal suction further
increases susceptibility to infection.
 In addition, the normal heat and moisture exchanging
mechanisms are bypassed requiring artificial
humidification of inspired gases.
 Failure to provide adequate humidification increases the
risk of sputum retention and infection.

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 Acid –base disturbance

 Ventilating patients with chronic respiratory failure or

hyperventilation may, by rapid correction of
hypercapnia, cause respiratory alkalosis.
 This reduces pulmonary blood flow and may contribute
to hypoxaemia.
 A respiratory acidosis due to hypercapnia may be due to
inappropriate ventilator settings or may be desired in an
attempt to avoid high VT and ventilator trauma.

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 Water retention
 Vasopressin released from the anterior pituitary is
increased due to a reduction in intrathoracic blood
volume and psychological stress.
 Reduced urine flow thus contributes to water retention.
In addition, the use of PEEP reduces lymphatic flow with
consequent peripheral oedema, especially affecting the
upper body.
Respiratory muscle wasting

 Prolonged ventilation may lead to disuse atrophy of the

respiratory muscles.

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