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Basic physics related to mechanical ventilation
Chatburn's classification of ventilators
Modes of ventilation
Ventilator settings and alarms
Ventilator induced lung injury
High frequency ventilation
Ventilation of the patient with unilateral lung disease
Partial liquid ventilation
Prone ventilation
Weaning
Further reading
Basic physics related to mechanical ventilation
In simple terms the lung-ventilator unit can be thought of as a tube with a
balloon on the end with the tube representing the ventilator tubing, ET tube and
airways and the balloon the alveoli.
- Pressure at point B is equivalent to the alveolar pressure and is
determined by the volume inflating the alveoli divided by the compliance of the
alveoli plus the baseline pressure (PEEP)
- Pressure at point A (equivalent to airway pressure measured by the
ventilator) is the sum of the product of flow and resistance due to the tube and
the pressure at point B.
- Flow, volume and pressure are variables while resistance and
compliance are constants.
- Flow = Volume/time
- It follows from the
relationships between pressure, flow and volume that by setting one of pressure,
volume or flow and the pattern in which it is delivered (which includes the time
over which it is delivered) the other two become constants.
- It also follows that
it is not possible to preset more than one of these variables as well as time.
Thinking of the lung-ventilator unit in terms of this simple model is also
useful in aiding an understanding of the use of monitoring end-inspiratory pause
pressure. In volume and flow preset modes pressure becomes a dependent variable.
It is important to monitor pressure in order to minimize the risk of barotrauma.
However, in this context it is alveolar pressure not airway pressure that is
important. By measuring the airway pressure during an end-inspiratory pause it
is possible to eliminate the component due to resistance because during an end-inspiratory
pause there is no flow and thus PAW=PALV. In most
circumstances the contribution of the resistance component to airway presssure
is relatively small and constant so it is reasonable to monitor airway pressure,
however in patients with high resistance (eg patients with obstructive lung
disease) it is important to monitor end-inspiratory pressure. Measurement of
end-inspiratory pressure may also help determine the cause of a sudden rise in
airway pressure. If both are high then the problem is due to a fall in
compliance (eg endobronchial intubation, pneumothorax) while if only the airway
pressure is high then the problem is due to increased resistance (eg partially
blocked ETT, bronchospasm)
Chatburn's classification of ventilators
- uses a framework of power source, drive mechanism, control mechanism and
output
- ventilator's functional characteristics are basically described by control
mechanism and output
Control mechanism
- pressure, volume and flow are variables. Compliance and resistance are
constants
Variable and waveform control
If any one of the variables and its resultant waveform can be preset the
other 2 variables become dependent variables. If none can be preset the
ventilator is a time-controller
- pressure control: ventilator applies a set pressure with a set waveform. Flow
and volume will depend on compliance, resistance and the pressure waveform
chosen
- flow control: ventilator delivers a set flow rate and pattern independent of
patients respiratory mechanics and hence resultant volume is also constant.
Pressure depends on flow rate and pattern, volume or inspiratory time, and
respiratory system mechanics
- volume control: volume constant but specific measurement of volume
distinguishes this from flow control
- time control: only inspiratory and expiratory times are controlled
Phase variables
- trigger variables
- variable used to initiate inspiration
- eg fall in airway pressure or loss of basal flow (flow-by-trigger mode).
During flow-by a continuous flow of gas is presented to the patient and is
vented in toto through the expiratory tubing unless the patient makes an
inspiratory effort. Machine senses any difference in this basal flow and the
actual flow in the expiratory limb and this triggers a mechanical breath.
The difference required depends on the sensitivity setting, usually 1-3
L/min.
- pressure may be sensed at ventilator (underestimates effort) or at Y-piece
(delays sensing by transducer sited in ventilator) with no real benefit of
one over other
- for given time delay flow triggering offers no advantage over pressure
triggering but proper setting of flow sensitivities can reduce inspiratory
work
- degree of change in variable required to trigger inspiration altered by
sensitivity setting
- over sensitive settings will lead to autocycling
- limit variables
- flow, volume or pressure can be set to remain constant or reach a maximum
- may be same as or unrelated to variable that terminates inspiration (ie
cycle variable)
- eg preset inspiratory pressure is achieved in PSV but usually flow
terminates inspiration
- controversy as to whether flow should be volume or pressure limited
- former has advantage of delivery of a known tidal volume but this may be
at expense of high peak airway pressure
- latter: less risk of excessive peak pressures but may be fluctuations in VT and minute ventilation due to changes in impedance
- cycle variable
- variable used to terminate inspiration. In Europe and Australasia this is
most commonly time. However in the USA it is usually volume.
- baseline variable
- variable that is controlled during expiration
- pressure is most practical and common
Conditional variable
- some ventilators capable of delivering different patterns of pressure,
volume and flow depending on what conditional variables are met
- eg in SIMV a sensed patient effort and an open spontaneous phase
("window") will allow a spontaneous breath, otherwise a mandatory
breath is delivered
Pressure vs volume limiting
Decelerating flow pattern, seen in pressure limited or controlled
ventilation, is associated with improved gas distribution with improved
ventilation-perfusion matching, and thus improved oxygenation and decreased dead
space
Ventilator settings and alarms
High airway pressure
- in addition to providing alarm breath should be pressure limited and thus
patient will only receive part of the preset tidal volume
- if pressure limit is repeatedly exceeded patient should be disconnected and
manually ventilated while problem diagnosed. Initial steps are to check for ETT
blockage and ventilator malfunction. Other factors to consider are airway
resistance, pneumothorax, endobronchial intubation
- causes of high airway pressures include:
- Asynchronous breathing
- Low compliance (high peak and plateau pressures):
- endobronchial intubation
- pulmonary pathology
– pneumothorax
- hyperinflation: dynamic, obstructed PEEP valve or expiratory port,
excessive PEEP
- ascites
- Increased system resistance (high peak pressures only):
- obstruction to flow in circuit, tracheal tube
- malplaced ETT
– bronchospasm
- aspiration/secretions
- calculation of dynamic and static effective compliance may give indication
of cause of increased airway pressure. Dynamic effective compliance is actually
a measure of impedance as it consist of both compliance and resistance
components. Dynamic effective compliance = (Peak airway pressure-PEEP)/delivered
tidal volume. Static effective compliance=(Plateau pressure-PEEP)/delivered
tidal volume. Delivered tidal volume=Tidal volume-ventilator compressible
volume. PEEP=the higher of PEEPi and PEEPe
- dynamic effective compliance reduced by decreases in lung or chest wall
compliance or increases in airway resistance while static compliance is not
affected by resistance (assuming pressure measurement is made when there is no
flow)
- no specific airway pressure guaranteed to exclude risk of barotrauma. In fact
main determinant of alveolar overdistension is end-inspiratory volume rather
than pressure. However latter is easier to measure. Plateau pressure probably a
better estimate of peak alveolar pressure than peak airway pressure. Based on
animal studies and the knowledge that human lungs are maximally distended at a
respiratory system recoil pressure of 35 cm H2O maintaining plateau
pressure < 35 recommended. NB if pleural pressure increases (eg due to
distended abdomen) then plateau pressure will increase without an increase in
alveolar pressure
Tidal volume
Causes of low tidal volume in pressure preset modes:
- Asynchronous breathing
- Decreased compliance
- Increased system resistance
- Inadequate preset pressure
- Gas leak
Inspiratory flow
- = tidal volume/inspiratory time
- high flow rates result in high peak airway pressures. May not be of concern
provided that most of the added pressure is dissipated across the ETT. Patients
may find abrupt bolus of gas uncomfortable and "fight" ventilator
- low flows prolong inspiratory time and therefore increase mean airway pressure
which may improve oxygenation but at the risk of increasing RV afterload and
decreasing RV preload. Also decreases expiratory time and predisposes patient to
dynamic hyperinflation. Patient may find flow insufficient and begin to
"lead" the ventilator, sustaining inspiratory effort throughout much
of the inspiratory cycle
Expiratory flow
- cannot usually be set
- = tidal volume/expiratory time. Latter is difference between cycle time and
inspiratory time
- principal ventilator-related determinant of dynamic hyperinflation
Triggering
- flow/pressure triggering
- characterised by sensitivity and responsiveness (delay in providing
response)
- even with modern sensors there is unavoidable dys-synchrony due to the need
for a certain level of insensitivity to prevent artefactual triggering and
delay due to opening of demand valves
- strategies to minimize dys-synchrony:
- - ventilators with microprocessor flow controls often have significantly
better valve characteristics than those on older generation ventilators
– continuous flow systems superimposed on demand systems can improve demand
system responsiveness in patients with high ventilatory drive (but can reduce
sensitivity in patients with very low respiratory drive)
– flow based triggers ̃ more sensitive and
responsive breath triggering
– small amount of pressure support usually ̃
ventilators’ initial flow and may ̃ improved
response characteristics in CPAP
– setting PEEP below PEEPi may improve triggering in patients with COPD who
have an inspiratory threshold load induced by PEEPi.
Ventilator induced lung injury
Oxygen toxicity
- Probably not significant with FIO2<0.5
Barotrauma
Images
- Air leak from alveoli situated near respiratory bronchioles
Factors predisposing to barotrauma
- high airway pressures. High peak inspiratory pressures may simply be a
marker of low pulmonary compliance rather than a causal factor. Incidence of
barotrauma was similar in patients ventilated in CMV and HFV modes in one study
of 309 patients with acute respiratory failure
- frequent positive pressure breaths
- pulmonary infection
- systemic infection
- diffuse pulmonary injury (ARDS)
- hypovolaemia
Warning signs
- PIP > 40 cmH2O
- pulmonary interstitial emphysema on CXR. May be difficult to detect. Manifests
as small parenchymal air cysts, air patterns that fail to taper toward the
peripheral lung margins and haloes or crescents surrounding pulmonary vessels
- subpleural air dissection producing linear collections of air or frank air
cysts
- mediastinal emphysema
- abrupt increase in PADP (8-12 mmHg)
Management of patients with pulmonary barotrauma
- pneumothoraces require drainage
- tension pneumomediastinum may cause cardiovascular collapse and require
decompression. Patients may complain of chest pain and ECG changes may be
present; may confuse diagnosis. Hamman's sign ("mediastinal crunch")
present in up to 50% In infants can be achieved by insertion of a small catheter
into anterior mediastinum while in adults most efficient method is to make an
incision 2-3 cm cephalad to suprasternal notch and open deep fascia beneath
sternum. Tension pneumomediatinum unusual because decompression into pleural
cavity and subcutaneous tissues usually occurs first.
- pneumopericardium may require immediate treatment if cardiac tamponade occurs.
Treat with pericardiocentesis
- important to maintain adequate ventilation without contributing to additional
morbidity and mortality. Mortality from acute respiratory failure ranges from
20-80% while barotrauma related mortality is <1%. Thus make every effort to
maintain oxygenation through increased expiratory pressure (PEEP/CPAP) and
increased Fio2 while reducing the number of mechanical breaths
Volutrauma
- Experiments with negative pressure ventilation have demonstrated that
excessive stretch in the absence of excessive airway pressure can cause lung
injury
- Trend is towards using smaller tidal volumes (7-10 ml/kg instead of 10-15
ml/kg) ARDSnet
study showed tidal volumes of 4-8 ml/kg are associated with an improved
outcome in patients with ALI or ARDS.
Shear stress
- Collapse and re-opening of alveoli with each tidal breath results in
continual shear stress
- This is thought to play a part in ventilator induced lung injury and is the
theoretical basis for use of high PEEP (above lower inflection point of static
pressure volume curve).
High frequency ventilation
- def: ventilation of lungs at a frequency > 4 times normal rate
- most important difference from conventional IPPV is that it requires tidal
volumes of only 1-3 ml/kg body weight to achieve normocarbia
- 3 types: high frequency positive pressure (used in anaesthesia), high
frequency jet (anaesthesia and ICU) and high frequency oscillation
Proposed advantages
- reduced peak and mean airway pressures
- improved CVS stability due to above
- decreased risk of barotrauma
- allows adequate ventilation with a disrupted airway (eg bronchopleural
fistula)
- permits mechanical ventilation during bronchoscopy
- improves operating conditions eg in thoracic surgery
- allows ventilation through narrow catheters and thus increases access during
laryngeal and trachael surgery
- reduces sedation requirements when used in ITU
- avoidance of hypoxia during tracheobronchial toilet
Disadvantages
- specialized equipment required
- dangers of high pressure gas flows
- humidification of inspired gases difficult
- tidal volumes markedly affected by changes in respiratory compliance
- monitoring of ventilation parameters difficult
- difficult to predict minute ventilation from ventilator
High frequency jet ventilation
- pulses of gas delivered at high velocity through an orifice at frequency of
10-100 Hz
- orifice may be in a T-piece connected to a conventional ETT, in a narrow tube
incorporated in wall of a special ETT or at end of fine bore catheter placed in
trachea
- in early part of inspiratory cycle jet entrains gas. Entrained gas develops a
normal flow profile which acts as a piston in trachea
- expiration is passive
- essential to have a free expiratory pathway to prevent barotrauma
- entrained gas can be humidified
- behaves like a constant pressure generator in that tidal volume is dependent
on compliance
- probably useful in barotrauma and in patients with a gas leak eg
bronchopleural fistula
- may improve haemodynamic status of patient if it leads to a reduction of
airway pressure
- ? of benefit in ARDS in combination with other methods of decreasing
barotrauma
High frequency oscillation
- both inspiration and expiration are active
- piston or loud-speaker cone used to produce a sinusoidal pattern of
respiration in which expiration is mirror image of inspiration
- frequencies: 2-100 Hz
- an auxillary flow of gas (bias flow) crosses the oscillating gas flow to
provide fresh gases and clear CO2
- behaves like a T-piece: efficiency of CO2 removal is a function of
bias gas flow
- stroke volume of oscillator is less than anatomical dead space
- mechanism of gas exchange is not clear
- used principally in neonates with RDS. Little evidence to suggest it is
superior to conventional ventilation
Mechanisms of gas exchange
- direct alveolar ventilation: tidal volumes of as low as 1 ml/kg still
result in direct ventilation of centrally situated alveoli
- enhanced diffusion: due to increased turbulence and convective mixing
- Pendelluft: adjacent lung units show asynchronous filling and emptying with
slow units filling from fast units
- acoustic resonance: ? produces resonant waves which cause turbulence
- cardiogenic mixing: mixing due to mechanical interaction of heart beating
against lung
- molecular diffusion
Ventilation of patients with unilateral lung disease
- in unilateral lung injury (eg following trauma, aspiration and pneumonia)
ventilation may go primarily to normal lung. If high pressures and volumes are
used this may result in:
- overdistension of normal lung with resultant barotrauma and volume trauma
and elevation of VD/VT
- shunting of blood away from the good lung resulting in increased shunt
Conventional mechanical ventilation
- beware overdistension
- consider Ư inspiratory time and decelerating
flow profile
Lateral positioning
- unaffected lung dependent̃
- ß shunting but
– risk of spillage into good lung
Independent lung ventilation
Picture
Criteria: 1 of the following:
- ß PaO2 refractory to high FIO2
and PEEP (PaO2/FIO2 ratio <150)
- PEEP induced deterioration in oxygenation or shunt fraction
- Over-inflation of non-involved lung
- Significant deterioration in circulatory status in response to PEEP
Technique
May be synchronous or asynchronous. The latter allow each lung to be
considered as an independent entity, simplifying management. Different modes,
rates, pressures and volumes can be used on each side. Even different
ventilators can be used. Cardiovascular problems associated with asynchronous
ventilation are insignificant. PA and PAWP difficult to interpret but cardiac
output and systemic pressures unchanged from pre-independent lung ventilation.
Ventilation should be titrated against blood gases and pressures/volumes
obtained from each ventilator.
Partial liquid ventilation
- Still an experimental technique
- Lung is partially filled with perfluorocarbon and patient is ventilated with
conventional apparatus
- Perfluorocarbons are simple organic compounds in which all the hydrogen
atoms have been replaced by halogens. There physicochemical properties include
high density, relatively high viscosity, low surface tension and a remarkable
ability to dissolve both oxygen and carbon dioxide
- Partial liquid ventilation results in improved gas exchange due to ß
shunt and Ư compliance. Because of the higher
density of perfluorocarbons compared to lung tissue and to alveolar fluid
perfluorocarbons are able to penetrate and re-expand dependent collapsed
alveoli. Due to gravity perfluorocarbons are preferentially distributed to
dependent areas which correspond to areas of colllapse in acute lung injury.
- Improvement in compliance may simply be due to recruitment of alveoli but
may be also be due to a direct effect on surface tension
- Other postulated benefits:
- barrier against infection
– washes out inflammatory debris
Prone ventilation
- 50-75% of patients with ARDS (and some other causes of acute respiratory
failure) show an improvement in oxygenation when turned prone
- probable mechanism is that when patient is turned prone the ventilation to
the dorsal atelectatic parts of the lung is improved. However perfusion
continues to pass preferentially to these regions and hence shunt is reduced
- improvement in gas exchange often persists even patient is returned to
supine position. This is probably because once the collapsed alveoli have been
recruited in the prone position they can be kept open by PEEP
- reduction in thoraco-abdominal compliance thought to play an important
part in producing beneficial effects of prone ventilation
- most common serious complication of turning prone is accidental extubation
Weaning
- process by which ventilator-dependent patient is removed from ventilator
- only 10-20% of patients who require ventilation are difficult to wean and most
of these have required ventilation for over 1 month
- potentially reversible reasons for difficult weaning:
- inadequate respiratory drive
- poor gas exchange
- psychological dependency
- ventilatory pump failure (usually due to inspiratory muscle weakness or
fatigue)
- causes for inspiratory muscle weakness or fatigue:
- NB mechanical ventilation may not necessarily rest respiratory muscles
- no objective rigorously generated data to determine when it is prudent to
attempt weaning. In general the problem which led to the initiation of
mechanical ventilation should have been reversed or stabilized
- many indices have been used to predict ability to totally discontinue
mechanical ventilation. Note that these indices do not indicate when to start
weaning process only indicate day on which complete discontinuation is likely to
be successful. Of these indices the most useful is Yang and Tobin’s rapid
shallow breathing index. This is obtained by dividing the respiratory rate in
breaths/minute by tidal volume in litres. A value of £
105 has a positive predictive value of 0.78 and a negative predictive value of
0.95 for prediction of weaning success. NB Tidal volume needs to be measured
using a spirometer rather than by using ventilator derived value. Predictive
value of the index is greatly reduced if ventilator derived figures are used
- standard criteria for initiating weaning:
- clinically and radiologically resolving lung disease: PaO2>8 kPa on
FiO2 <0.4 and < 10 cm PEEP
- PaCO2 <6 kPa
- RR < 30/min
- minute volume >10 L/min
- patient awake and cooperative
- VC > 15 ml/kg
- max inspiratory pressure > -25 cm H2O
- optimal methods for weaning are probably once daily T-piece trial or
pressure support weaning. Once daily T-piece trials are preferable to multiple
short trials, probably because fatigued respiratory muscles are given sufficient
time to recover between trials. May take 24 h for recovery.
- criteria for failure of weaning trial (either t-piece or decreased level of
pressure support) are based on clinical assessment of the development of fatigue
or clinical deterioration eg HR 30/min above baseline, MAP 15 mmHg above or 30
mmHg below baseline, arrhythmias, RR > 35 for 5 mins, SpO2<90%,
patient dypnoea score ³ 5/10
- note that discontinuation of mechanical ventilation results in an increase
in preload and afterload. Development of left ventricular failure as a result of
this is an important cause of failure to wean.
Further reading
Albert, R.K. For every thing (turn...turn...turn....).
Am.J.Respir.Crit.Care Med 155:393-394, 1997.
Antonelli, M., Conti, G., Rocco, M., Bufi, M., De Blasi, R.A., Vivino, G.,
Gasparetto, A., and Meduri, G.U. A comparison of noninvasive positive-pressure
ventilation and conventional mechanical ventilation in patients with acute
respiratory failure. N.Engl.J.Med 339(7):429-435, 1998.
Esteban, A. and Alía, I. Clinical management of weaning from mechanical
ventilation. Intens.Care Med. 24:999-1008, 1998.
Hilbert
G et al. Noninvasive ventilation in immunosuppressed patients with pulmonary
infiltrates, fever, and acute respiratory failure. N.Engl.J.Med 344
(7):481-487, 2001.
MacIntyre N. Improving patient/ventilator interactions. In Vincent J-L. (ed)
Yearbook of Intensive Care and Emergency Medicine 1999. Springer-Verlag, Berlin,
1999; pp234-243
Pinsky, M.R. The hemodynamic consequences of mechanical ventilation: an
evolving story. Intens.Care Med. 23:493-503, 1997.
Slutsky AS. Consensus conference on mechanical ventilation - January 28-30,
1993 at Northbrook, Illinois, USA. Part 2. Intensive Care Med 1994; 20:150-162
© Charles Gomersall July 1999
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