Anaesth Intens Care (1986). 14.

226-235

Physiological Aspects of Intermittent

Positive Pressure Ventilation
D. R. HILLMAN*
Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Perth, Western Australia

SUMMARY
The mechanical properties of the lungs and chest wall dictate the relationship between tidal
volume, flow rate and airway pressure developed during intermittent positive pressure ventilation
(IPPV). The increase in intrathoracic pressures associated with IPPV has consequences for the
intrapulmonary distribution of ventilation and perfusion (hence gas exchange), cardiac output and
regional blood flows. Barotrauma is a potential hazard. IPPV also affects the homeostatic
mechanisms that keep the air spaces dry.
Strategies to maximise the benefits and minimise the side effects of IPPV include positive end-
expiratory pressure, intermittent mandatory ventilation, differential lung ventilation and high
frequency ventilation. .
Understanding the physiological effects of IPPV and associated therapies allows a rational
approach to the adjustment of ventilation against pulmonary, cardiovascular and systemic
responses so as to optimise gas exchange and peripheral oxygen delivery.

Key Words: LUNG: ventilation, IPPV, physiology, mechanical

To maXImIse the benefits of intermittent MECHANICAL PROPERTIES OF THE

positive pressure ventilation (IPPV), an RESPIRATORY SYSTEM
understanding is required of 1. how the The pressure gradient from the upper airways
inspiratory force generated by the ventilator to the alveoli necessary for inspiration is
interacts with the elastic and flow resistive provided by the creation of a negative
properties of the respiratory system to produce intrapleural pressure (by muscle activity) during
ventilation and gas exchange, 2. how these spontaneous ventilation, or a positive airway
elastic and flow properties may change with pressure during IPPV. In either case, the
mechanical ventilation, and 3. how the change distending pressure across the lung, the
from the negative inspiratory intrathoracic transpulmonary pressure (which is alveolar
pressures of spontaneous breathing to the pressure minus intrapleural pressure),
positive pressures of IPPV affects increases.
cardiovascular and other organ systems. Only The driving pressure required to produce a
by understanding these physiological given tidal volume and inspiratory flow rate is
consequences may the therapeutic goal of determined by the passive forces that must be
adequate ventilation, gas exchange and overcome. Hence during IPPV, the inflation
peripheral oxygen delivery be achieved with pressure is equal to the sum of the pressures
minimal side-effects. required to overcome elastic, flow resistive, and
(less importantly) the inertial properties of the
lungs and chest wall.
*F.F.A.R.A.C.S .• Clinical Physiologist.
Address for Reprints: Dr. D. R. Hillman. Department of Pulmonary
The pressure gradient required to overcome
Physiology, Sir Charles Gairdner Hospital, Nedlands. Western Australia 6009. the elastic recoil of lungs and chest wall is equal
Anaesthesia and Intensive Care, Vol. 14, No. 3, August, /986
 IPPV PHYSIOLOGY 227

to the volume increase above functional calibre is very important in determining the
residual capacity (FRC) divided by the total magnitude of airway resistance.
respiratory compliance. By assuming laminar Airway calibre may be decreased by
flow (see later), the pressure gradient required intraluminal obstruction (e.g. secretions,
to overcome resistive forces is equal to the blood, foreign body or tumour), inflammation,
product of flow rate at the instant of oedema, increase in airways smooth muscle
measurement and total respiratory resistance. tone, external compression, or loss of external
Under conditions of zero flow (e.g. at end- elastic support (as in emphysema). The elastic
inspiration), the pressure gradient is entirely recoil of surrounding tissues tends to hold
due to elastic forces. airways open. Airways calibre is greatest at
Lung elastic recoil is attributable to surface TLC where elastic recoil is greatest, and at least
tension and tissue elasticity. Surface forces vary at residual volume at which point significant
enormously - surface tension is greatest at airways closure has occurred, particularly in the
high lung volumes, decreasing progressively dependent portions of the lung. An increase in
with lung deflation to relatively low values at lung volume, as produced by positive end-
50070 total lung capacity (TLC). I Surfactant, a expiratory pressure (see later) or by tonic
detergent-like substance lining the alveoli, inspiratory muscle contraction (e.g. in asthma),
reduces surface tension. A deficiency in allows increased respiratory flows by increasing
surfactant greatly decreases lung compliance elastic recoil in the tissues surrounding airways.
and is seen in the neonatal respiratory distress As seen above, many conditions may either
syndrome. Lung tissue elastic recoil may also be increase respiratory resistance or decrease
altered by disease. Compliance is decreased by compliance and thus necessitate an increase in
pulmonary infiltration, oedema, fibrosis, driving pressure to maintain adequate
atelectasis and pleural disease, whereas it is ventilation. The consequence for spontaneous
increased by parenchymal destruction (e.g., ventilation will be an increase in muscle work,
emphysema). predisposing to fatigue, and for IPPV, an
increase in airway pressure with greater
Chest wall compliance is decreased by muscle potential for undesirable effects as discussed
tone, obesity, abdominal distension, external later.
factors (such as tight bandages, clothing and
weights on the abdomen or rib cage), and INFLUENCE OF LUNG AND CHEST WALL
diseases or deformations of the rib cage (such PROPERTIES ON MECHANICAL VENTILATION
as ankylosing spondylitis and kyphoscoliosis). The mechanical properties of the lungs and
Total respiratory resistance reflects the chest wall (i.e. their compliance and resistance)
frictional forces developed during airflow and determine the flow rate produced by a
movement of tissues. Of the total pulmonary constantly applied pressure (such as by a
resistance, more than 90% is attributable to air pressure-generator ventilator 2) and the
flow resistance and less than 10% to tissue flow proximal airway pressure produced by any
resistance. applied flow pattern (such as by a flow-
The magnitude of airflow resistance depends generator ventilator2).
on whether the flow is laminar (in which case Inspiratory time is decreased by increasing
driving pressure is proportional to flow rate) or the applied pressure in the case of a pressure-
turbulent (in which case driving pressure is generator ventilator, or by increasing the
proportional to the square of flow rate). Flow is applied flow rate in the case of a flow
transitional in most of the bronchial tree, with generator.
eddy formation where branching occurs. In The tidal volume delivered by a ventilator
general, driving pressure is proportional to depends on the mechanical properties of the
both flow rate and its square. For laminar flow, lungs and the magnitude and duration of the
resistance is inversely proportional to the applied pressure. Inspiratory to expiratory
fourth power of airway radius, and for cycling of the ventilator may be based on a
turbulent flow, it is inversely proportional to predetermined time, airway pressure, tidal
the fifth power of airway radius. Hence airway volume or inspiratory flow rate. A pressure-
Anaesthesia and Intensive Care, Vol. /4, No. 3. August, 1986
228 D. R. HILLMAN

generator, time-cycled ventilator will deliver a frequency. In the former case, excessively short
decreased tidal volume in the face of increased inspiratory times may result in an increased
respiratory resistance or decreased compliance. maldistribution of ventilation (see below). In
Under these circumstances, a flow-generator, the latter case, if tidal volume is held constant,
time-cycled ventilator will deliver nearly, if not hypoventilation Play result from too low
precisely, the same tidal volume but airway respiratory rates. A degree of hypoventilation
pressure will be increased. may be accepted when ventilating asthmatics,
In a pressure-generator, volume-cycled in an effort to gain a sufficiently long
ventilator, inspiratory time will become expiratory time.
prolonged in the presence of increased INTRAPULMONARY GAS DISTRIBUTION
resistance or decreased compliance. If We have so far considered the overall
sufficient changes in these properties occur, the mechanical properties of the lungs and chest
applied pressure may not be enough to wall and their effects on ventilation. However,
overcome these passive forces and cycling will these properties are not evenly distributed.
cease. In a flow generator, volume-cycled Non-homogenous lung disease or IPPV may
ventilator, the above abnormal lung properties disturb the intrapulmonary distribution of
will result in an increased inspiratory airway ventilation, resulting in ventilation-per fusion
pressure. Where pressure cycling is employed, mismatch, and hence, disordered gas exchange.
the same abnormalities will cause the ventilator
TLC
to reach the pre-set cycling airway pressure
early, with a consequent decrease in tidal
volume and increase in respiratory frequency.
.•
The inspiratory flow wave form varies "a
>
according to ventilator design. A constant ...
pressure generator develops a square wave ""
...J
proximal airway pressure - the inspiratory
flow is maximal early and decreases
exponentially as elastic recoil forces increase RV
with the increase in intrathoracic volume. A
constant flow generator develops a constantly
increasing proximal airway pressure during
inspiration. Sine wave flow generators, such as Tran.pulmonary Pr ••• ur.
those based on a cylinder and piston, develop a FIGURE I.-Diagrammatic representation of the volume-
sinusoidal inspiratory flow. Other wave forms pressure curve of the lung between total lung capacity
may' be generated by appropriate ventilator (TLC) and residual volume (RV). The curve has a sigmoid
design. Although various flow patterns have shape. Near RV (a) and TLC (c) the curve is flatter than
between these limits (b). Hence the same distending
been advocated,3.8 there is no convincing pressure produces smaller volume changes at (a) and (c)
evidence to suggest that any particular wave than at (b).
form is superior.
Expiration in a ventilated patient generally In normal lungs, the distribution of
occurs by passive means. The pressure gradient ventilation is determined by the vertical
from alveoli to atmosphere is generated by the gradient in pleural pressures and (provided the
elastic recoil of the lungs and chest wall, inspiratory flow rate is low), by the static elastic
opposed by airway resistance. Hence where properties of the lung units.9,1O The gradient in
airway resistance is increased and/or pleural pressures (being lowest in the
compliance is decreased, expiration may be nondependent regions) is the result of gravity
prolonged. Air trapping and progressive and the shape of the chest wall. I1 Hence, the
hyperinflation will occur if insufficient time dependent regions of the lung are normally on a
elapses before the next inspiratory cycle. This steeper part of the lung volume-pressure curve,
may be avoided by setting an adequate time for which becomes progressively flatter at higher
expiration - either by reducing the inspiratory- distending pressures (Figure 1). Consequently
to-expiratory time ratio or the respiratory dependent lung units undergo a larger volume
Anaesthesia and Intensive Care. Vol. 14. No. 3, August. 1986
 IPPV PHYSIOLOGY 229

change for a given change in pleural pressure As per fusion is vertically distributed,
(i.e. they are more compliant than ventilation and perfusion remain well matched.
nondependent units). This vertical gradient in The supine posture in the awake, spontaneously
pleural pressures is modified by the pattern of breathing patient is similarly associated with
respiratory muscle activity which changes the greater diaphragmatic movements in the
shape of the chest wall and regional pleural dependent zones. 14
pressure gradients. 12 IPPV in the supine position results in
Pulmonary perfusion is also vertically changes in the mechanical properties of lungs
distributed, as a result of gravity. Hence the and chest wall, which in turn alter the
distribution of ventilation and perfusion are distribution of ventilation, so that preferential
normally well matched. ventilation of the dependent zones no longer
As inspiratory flow rates increase, time occurs. A decrease in functional residual
constants throughout the lung assume a greater capacity (FRC) is seen, the mechanism of which
influence on the distribution of ventilation than is not fully understood. It appears to be largely
static elastic properties. The time constant of a due to a change in the volume-pressure
lung unit is given by the product of its characteristics of the chest wall 15 with cephalad
compliance and resistance, and determines the displacement of the diaphragm and loss of lung
rate of inflation for any particular inflation volumes, both occurring predominantly in
pressure. It denotes the time taken for that dependent zones. 14-16 A consequence of this loss
region to reach 1. its final volume after the of lung volume is the development of
appfication of a flow, if the initial rate of flow microatelectasis (accelerated by the use of high
has been maintained, or 2. 63070 of its final oxygen concentrations I), with increased right
volume, if the applied pressure was held to left intrapulmonary shunting. The loss of
constant and assuming an exponential decrease lung volume causes the dependent regions
in flow with increase in volume. In pulmonary (which are already at a lower volume) to move
disease where greater variation and to a still lower, flatter portion of their volume-
prolongation of regional time constants exist pressure relationships, with a resultant decrease
(e.g. obstructive airways disease), inspired gas in compliance relative to nondependent regions
is preferentially distributed to those alveoli with (Figure 1).
short time constants. This tendency to uneven The decrease in ventilation of the dependent
distribution is accentuated by increasing zones during IPPV is also caused by changes in
inspiratory flow rates. 13 A pause at the end of diaphragmatic displacement. During IPPV, the
such an inspiration, however, allows a diaphragm is displaced by a relatively uniform
redistribution of inspired gas from alveoli with applied pressure which is opposed by a
a short time constants to those with longer time nonuniform, gravity-dependent, hydrostatic
constants. pressure gradient generated by the abdominal
Posture and the effects of sedation and contents, with the result that diaphragmatic
paralysis are important in the consideration of displacement is greater in nondependent
intrapulmonary gas distribution in the regions. While preferential ventilation of the
mechanically ventilated patient. nondependent lung occurs during IPPV, the
In the awake, spontaneously breathing perfusion remains preferentially distributed to
patient, the lateral posture is associated with a dependent zones, hence ventilation-perfusion
decrease in volume of the dependent lung, mismatch occurs.
because the lower hemidiaphragm is displaced The application of positive end-expiratory
cephalad by the weight of abdominal contents. pressure (PEEP, see later) reduces the
This domed hemidiaphragm has an increased preferential ventilation of the nondependent
mechanical advantage relative to the flatter, lung by increasing the volume of the lungs, and
upper hemidiaphragm. It allows the dependent shifting dependent zones to a higher, steeper
lung to undergo a greater volume change with (more compliant) portion and non dependent
each diaphragmatic contraction and zones to a still higher, flatter portion of their
consequently, preferential ventilation of the respective volume-pressure relationships. 16 The
lower lung resuIts.I4 decrease in the airway closure and atelectasis
Anaesthesia and Intensive Care, Vol. 14, No. 3, August, 1986
230 D. R. HILLMAN

and the improved ventilation perfusion the shunted mixed venous blood will be more
matching following PEEP, reduces the degree desaturated. 21
of right to left intrapulmonary shunting. 18
BAROTRAUMA
GAS EXCHANGE
Pulmonary barotrauma results from
Efficient gas exchange is dependent on ideal overdistension of terminal and respiratory
matching of ventilation and perfusion at bronchioles and alveoli, with subsequent
alveolar level, absence of anatomical shunts, rupture into the perivascular sheaths of
and unimpaired diffusing capacity of the adjacent vessels. This extra-alveolar air may
alveolar-capillary interface. further dissect to the mediastinum, fascial
Abnormalities of gas exchange are most planes of the head and neck, pleural cavity,
commonly attributed to mismatching of pericardium, retroperitoneal regions, and over
ventilation and per fusion within the lung. We the pleural reflections of the great vessels. 22,23
have already seen that IPPV decreases the The pulmonary mechanical factors influencing
efficiency of gas exchange by altering the the magnitude of intrathoracic pressure
intrapulmonary distribution of ventilation. changes with ventilati0n have already been
IPPV may also impair gas exchange by an discussed. The elevated airway pressure
effect on alveolar perfusion. As pulmonary associated with mechanical ventilation and
vascular perfusion depends on the balance PEEP increases the incidence of
between pulmonary arterial pressure and barotrauma. 24,25 The critical determinant is the
alveolar pressure, a decreased pulmonary increased pressure gradient from alveolus to
arterial pressure and/or an increased alveolar interstitial space. This gradient is also increased
pressure, would be associated with a decrease in by pulmonary interstitial pressure: Lenaghan et
perfusion. Indeed, in areas of the lung where al. demonstrated that pneumothorax occurs at
alveolar pressure exceeds pulmonary arterial lower airway pressures in hypovolaemic than in
pressure, no perfusion takes place. A gravity- normovolaemic dogs. 26
dependent, vertical distribution of pulmonary CARDIOV ASCULAR FUNCTION
vascular pressures (and thus perfusion) exists. We have so far considered the effects of
Hence in nondependent lung zones, where mechanical ventilation on the lungs.
pulmonary arterial pressures are least, IPPV Cardiovascular function may also be affected,
(particularly with the addition of PEEP) may further influencing peripheral oxygen delivery,
lead to alveolar hypoperfusion and an increase as this is dependent on both arterial oxygen
in alveolar dead space. 19 ,20 The effect is content and cardiac output.
increased with high inflation pressures, or with Cardiac output usually decreases with the
conditions that decrease pulmonary arterial application of IPPV27 in part due to decreased
pressure (e.g. hypovolaemia). venous return. The decrease correlates directly
The potential adverse effect of PEEP on gas with the increase in intrapleural pressure, as
exchange by its effects on pulmonary perfusion right ventricular filling pressure equals right
is usually small relative to its beneficial effects ventricular end-diastolic pressure minus pleural
on intrapulmonary gas distribution, provided pressure. A decrease in lung compliance has a
excessive increases in inflation pressures or protective effect in that pleural pressure is less
decreases in right heart output are avoided (see elevated at the same airway pressure (i.e.
below). transpulmonary pressure is higher). Right heart
The associated use, during IPPV, of drugs output is also decreased during inspiration by
which decrease hypoxic pulmonary pulmonary microvascular compression which
vasoconstriction (such as volatile anaesthetic increases right ventricular afterload. 28 These
agents), will exaggerate the degree of depressant effects on right ventricular function
ventilation-perfusion mismatch. may be minimised by adequate intravascular
It should be noted that any decrease in fluid support. 28
cardiac output occurring in association with The decrease in right ventricular output
IPPV will increase the alveolar-arterial oxygen decreases left ventricular preload, and hence,
tension gradient in the presence of a shunt, as left ventricular output. There is also a
Anaesthesia and Intensive Care. Vol. 14, No. 3, August, 1986
 IPPV PHYSIOLOGY 231

mechanism which decreases left ventricular influencing interstitial pressure. Any increase in
output with the application of IPPV and PEEP surface tension tends to cause alveolar collapse
independent of changes in pleural pressure. It which lowers interstitial pressure by pulling the
appears to be related to increasing lung volume adjacent walls of the interstitial space away
as cardiac output is depressed if pleural from each other. An increase in transudation
pressure is held constant and lung volume is and interstitial oedema results.
allowed to increase. Suggested mechanisms Mechanical ventilation can influence this
include altered volume-pressure characteristics balance of forces. Ventilation with large tidal
of the left ventricle, secondary to right volumes increases surfactant turnover, 36
ventricular enlargement or external pressure on possibly by breaking up the surface film or
the ventricle by distended lungs. 29 It should be mechanically pumping surfactant out of the
noted that IPPV may also decrease stroke alveoli. An increase in surface tension with
volume and cardiac output by producing decreased compliance and interstitial oedema
hypocarbia. 30 may result. These changes may be important in
While the dominant haemodynamic effect of the aetiology of 'respirator lung'. The addition
IPPV is the decrease in right and left of PEEP provides some protection: 36,37 possible
ventricular performance, a less appreciated mechanisms include a decrease in the pumping
effect is an increase in left ventricular stroke effect seen at low lung volumes by increasing
volume during early inspiration. This is in part FRC, augmented surfactant production by the
attributable to left ventricular compression by continuous mild alveolar distension it induces,
the rise in intrathoracic pressure. It may also be or mechanical stabilisation of the surfactant
a consequence of decreased left ventricular film. Conversely, mechanical ventilation,
afterload due to an increase in pressure gradient optimally with PEEP, increases alveolar and
between intra- and extrathoracic vascular interstitial pressure, decreasing the hydrostatic
beds. 31 This mechanism appears to be pressure gradient. 38 This, together with the
important in some patients with poor left associated decrease in venous return and
ventricular reserve whose cardiac output recruitment of collapsed air spaces,39 makes
improves with IPPV. 32 IPPV with PEEP a useful therapy in
The rise in intrathoracic pressure affects pulmonary oedema, especially when caused by
regional blood flow, largely as a consequence increased pulmonary capillary pressures.
of its effect on cardiac output. Reflex mediated Several workers have found that PEEP
changes in the distribution of cardiac output act increases, rather than decreases, lung water in
to minimise the decrease in flow to vital isolated or experimental lungs. 40 ,41 Hence,
organs. 33 These effects of raised intrathoracic PEEP may improve gas exchange in pulmonary
pressure and its effect on intracranial pressure oedema principally by increasing alveolar
will be discussed further under 'positive end- volume rather than by reducing lung water.
expiratory pressure' .
PULMONARY OEDEMA AND IPPV STRATEGIES TO MAXIMISE BENEFITS AND
While controversy exists,34 most theories of MINIMISE ADVERSE EFFECTS OF IPPV
the homeostatic mechanisms keeping air spaces 1. Positive end-expiratory pressure (PEEP)
dry are versions of the Starling hypothesis - IPPV is associated with a decrease in FRC, as
opposing vascular and osmotic pressures has already been discussed. In addition, many
produce a net filtration of fluid into the lung diseases may decrease FRC. Pulmonary
interstitium. Lymph drainage can cope with oedema and inflammation or airway
this flow until there is an approximate eightfold obstruction can cause alveolar filling and/or
increase,3s which may occur if the endothelium collapse with consequent right to left
becomes more permeable to plasma protein or intrapulmonary shunting. By maintaining a
if the capillary-interstitium pressure gradient is high distending pressure at end-expiration,
raised, either by an increase in capillary PEEP increases FRC, counteracting these
pressure above a threshold of 25 mmHg (3.3 influences. When PEEP is raised above a
kPa) or a decrease in interstitial pressure. threshold level (the critical opening pressure for
Surface tension is an important factor the lung unit concerned) inflation of collapsed
Anaesthesia and Intensive Care, Vol. 14. No. 3, August, 1986
232 D. R. HILLMAN
alveoli occurs. Improved ventilation to increases. The risk of barotrauma, which
previously poorly ventilated or collapsed alveoli appears to increase with the frequency of these
decreases intrapulmonary shunt with an peaks,23 is decreased, as is the risk of
improvement in arterial P02. A lower cardiovascular depression. This may allow
fractional inspired oxygen concentration (F102) higher levels of PEEP to be tolerated than when
may then be used in an attempt to avoid the IPPV alone is used, with the potential for
toxic effects associated with high further improvements in gas exchange. Other
concentrations. 42 In non-homogeneous lung potential advantages include a more uniform
disease, excessive PEEP may lead to intrapulmonary gas distribution consequent
overdistension of normal alveoli, with a upon spontaneous breathing, less need for
decrease in perfusion of those alveoli (because sedatives and muscle-relaxants, a reduced
of vascular compression). The result is an tendency to respiratory alkalosis, and
increase in alveolar dead space and in right to facilitation of the weaning process by
left intrapulmonary shunting, as blood is graduated exercise of respiratory muscles. so
diverted to diseased non-ventilated lung zones. 3. Differential lung ventilation
Optimally, PEEP should be tailored to If there are gross discrepancies in the
maximise recruitment of alveoli while avoiding mechanical properties of each lung, then
overdistension .. Under this circumstance, separate ventilation of the lungs may be
measured overall pulmonary compliance undertaken via a double-lumen tube to avoid
should be maximal, and it has been preferential ventilation of the lung with the
recommended as an index to set the level of lower impedance. SI Differential lung ventilation
PEEP which would produce optimal gas may be either synchronous or asynchronous.
exchange. 43
The effects of IPPV and PEEP on cardiac 4. High frequency ventilation
output and regional blood flow have been High frequency ventilation is an alternative
discussed earlier. PEEP appears to decrease mode of ventilatory support to IPPV. Three
hepatic blood flow in proportion to the basic techniques exist: high frequency positive
decrease in cardiac output. 44 In addition, PEEP pressure ventilation, high frequency jet
decreases renal flow, urine output and sodium ventilation and high frequency oscillation. The
excretion: 4s possible mechanisms include a principle of these techniques is to allow
decrease in renal arterial blood flow secondary effective ventilation (by enhanced diffusion and
to decreased cardiac output,46 increased ADH interregional gas mixing) without high airway
secretion,47 and increased inferior vena caval pressures hence decreasing the risk of
compression. The use of low-dose dopamine barotrauma and cardiovascular depression.
infusions appears to counteract these effects. 48 The topic is covered in depth elsewhere in this
PEEP may increase intracranial pressure by symposium.
increasing central venous (and hence cerebral OPTIMAL VENTILATORY PATTERN
venous) pressure. This effect is not important Utilising the principles outlined above, an
when intracranial dynamics are normal, but approach may be made to the definition of an
when intracranial pressure is raised, PEEP may optimal pattern of IPPV.
produce significant further increases. 49 1. Tidal volume
A major potential problem with PEEP, as In normal lungs large tidal volumes (10-15
previously discussed, is pulmonary mllkg) tend to minimise right to left ventricular
barotrauma. The risk may be minimised by shunt. S2 However, in abnormal lungs with large
avoiding high peak airway pressures, for regional variations in compliance, gross
example by decreasing tidal volume as PEEP is overinflation of more normal regions may
increased. occur, thus increasing dead space. In this
2. Intermittent mandatory ventilation (IMV) situation, a combination of smaller tidal
IMV, by allowing spontaneous breathing volumes (5-10 mllkg) and PEEP is indicated to
between mandatory ventilator delivered recruit poorly ventilated and collapsed alveoli,
breaths, reduces average intrathoracic pressures thereby improving the distribution of
and the frequency of high peak airway pressure ventilation.
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 IPPV PHYSIOLOGY 233

2. Inspiratory flow rate, respiratory frequency monitoring may be useful. 55 Fluid loading
Rapid inspiratory flow rates have the and/or inotropic support may be needed.
potential to increase dead space by
preferentially ventilating lung units with short 6. Intermittent mandatory ventilation (IMV)
time constants (see above), and may thus be While controversy exists as to the choice of
undesirable. In general, slow rates (10-12 IMV versus continuous mechanical
breaths/minute) are indicated in adult patients. ventilation,56.57 IMV has several putative
An increase in respiratory rate to prevent advantages 50 outlined above which commend its
hypo ventilation would be indicated when high use, particularly in patients who are difficult to
tidal volume or peak inspiratory pressures are wean from IPPV.
undesirable. Conversely, an indication to 7. Fractional inspired oxygen concentration
decrease the respiratory frequency would be (F I0 2)
severe airflow obstruction, so as to allow The optimisation of the ventilatory pattern
sufficient time for expiration (hence avoiding and use of PEEP to minimise F 102 has already
air trapping and progressive hyperinflation). been discussed. In determining the balance
between FI02 and PEEP, it should be
3. Inspiratory flow pattern remembered that peripheral oxygen delivery is
Despite different inspiratory flow patterns dependent upon both arterial oxygen content
having been advocated by various sources and cardiac output.
outlined earlier 3.8 there appears to be no clear
8. Airway pressure
advantage to any particular pattern.
It is a principle of mechanical ventiiation to
4. Inspiratory to expiratory time ratio minimise peak and mean airway pressures, so
(I:E ratiop 3 as to reduce the risks of barotrauma and
This ratio should be sufficient to allow cardiac output depression respectively. The risk
adequate time for expiration and is generally of barotrauma is increased in certain conditions
less than 1: 1. In obstructive airway disease it (e.g. post-thoracotomy, obstructive airways
may be necessary to adopt an I:E ratio less than disease, and hypovolaemia). In general, a peak
1:3. airway pressure of less than 40 cm of water (5.3
kPa) should be aimed for.
5. PEEP
While understanding the physiological
PEEP is indicated when an adequate FI02
effects of IPPV allows a rational approach to
(generally considered to be 0.5) fails to
an optimal ventilatory pattern, rigid
maintain satisfactory oxygenation (e.g. arterial
application of principles to clinical practice is
P02 >60 mmHg or 8.0 kPa). As mentioned inappropriate. Each case requires a careful
previously, the use of PEEP may allow a lower
titration of the ventilatory pattern against the
FI02 to be used, thus reducing the risk of pulmonary, cardiovascular, and systemic
oxygen toxicity (which in adults appears to have
responses so as to optimise ventilation, gas
a FI02 threshold of approximately 0.642). exchange and peripheral oxygen delivery.
The usual range of PEEP employed is 5-15
cm of water. It is adjusted to maximise
REFERENCES
recruitment of alveoli while avoiding 1. Hoppin FG, Hildebrandt J. Mechanical Properties of
overdistension. 43 Predisposition to barotrauma the Lung. In: Bioengineering Aspects of the Lung. J
suggests that small tidal volumes (5-10 mllkg) West, ed. Dekker, New York, 1977.
should be used when PEEP is increased, to 2. Mapleson WW. In: Mushin WW, Rendel Baker L,
Thompson PW, Mapleson WW. Automatic
minimise peak airway pressure. The risk of Ventilation of the Lungs. Blackwell Scientific,
cardiac output depression increases with any Oxford, 1980.
increase in mean airway pressure and is not, 3. Bergman NA. Effects of varying respiratory wave
therefore, uniquely related to PEEP. The risk is forms on gas exchange. Anesthesiology 1967;
low when pulmonary compliance is low and the 28:390·395.
4. Norlander 0, Herzog P, Norden I et al. Compliance
patient is normovolaemic. 54 When the overall and airway resistance during anaesthesia with
margin of likely benefits over adverse effects controlled ventilation. Acta Anaesthesiol Scand 1968;
from PEEP is unclear, invasive haemodynamic 12: 136-152.
Anaesthesia and Intensive Care. Vol. 14. No. 3. August. /986
234 D. R. HILLMAN

5. Ingelstedt S, 10nson B, Nordstrom L, Olsson SG. A 23. Mathru M, Rao TLK, Venus B. Ventilator induced
servo controlled ventilator measuring expired minute barotrauma in controlled mechanical ventilation
volume, airway flow and pressure. Acta Anaesthesiol versus intermittent mandatory ventilation. Crit Care
Scand 1972; 47:Suppl:9-27. Med 1983; 11:359-361.
6. Baker AB, Thompson lB, Turner 1, Hansen P. Effect 24. Bone RC, Francis PB, Pierce AK. Pulmonary
of varying inspiratory flow waveform and time in barotrauma complicating positive and expiratory
IPPV; Pulmonary oedema. Br 1 Anaesth 1982; pressure. Am Rev Resp D 1975; 111:921.
54:539-46. 25. Peterson GW, Baier M. Incidence of pulmonary
7. Baker AB, Restall R, Cl ark BW. Effect of varying
barotrauma in a medical ICU. Crit Care Med 1983;
inspiratory flow waveform and time in IPPV:
11:67.
Emphysema. Br 1 Anaesth 1982; 54:547-54.
8. Al Saady N, Bennett ED. Decelerating inspiratory 26. Lenaghan R, Silva Yl, Wait Al. Hemodynamic
flow waveform improves lung mechanics and gas alterations associated with expansion rupture of the
exchange in patients on IPPV. Int Care Med 1985; lung. Arch Surg 1969; 99:339-343.
11:68-75. 27. Cournand A, Motley HL, Werko L et al. Physiologic
9. Milic Emili 1, Mead 1, Turner lM, Glauser EM. studies of the effects of intermittent positive pressure
Improved technique for estimating pleural pressure breathing on cardiac output in man. Am 1 Physiol
from oesophageal balloons. 1 Appl Physiol 1964; 1948; 152:162-174.
19:207 -211. 28. Qvist 1, Pontopiddan H, Wilson RS et al.
10. Bake B, Wood L, Murphy B et al. Effect of Haemodynamic responses to mechanical ventilation
inspiratory flow rate on regional distribution of with PEEP. Anesthesiology 1975; 42:45-55.
inspired gas. 1 Appl Physiol1974; 37:8-17. 29. Tyler DC. Positive end expiratory pressure: A review.
11. Mead 1. Mechanical properties of lungs. Physiol Rev Crit Care Med 1983; 11:300-308.
1961; 41:281-330. 30. Morgan BL, Crawford EW, Hornbein TF et al.
12. Fixley MS, Roussos CS, Murphy B, Martin RR, Engel Haemodynamic effects of changes in arterial carbon
L. Flow dependence of gas distribution and pattern of dioxide tension during intermittent positive pressure
inspiratory muscle contraction. 1 Appl Physiol 1978; ventilation. Anesthesiology 1967; 28:866-873.
45:733-741. 31. Robotham lL, Cherry D, Mitzner W et al. A re-
13. Woolcock Al, Vincent Nl, Macklem P. Frequency evaluation of the hemodynamic consequences of
dependence of compliance as a test for obstruction in IPPV. Crit Care Med 1983; 11:783-793.
the small airways. 1 Clin Invest 1969; 48:1097. 32. Mathru M, Rao TL, EI-Elr AA, Pifarre R.
14. Froese AB, Bryan AC. Effects of anesthesia and Hemodynamic response to changes in ventilatory
paralysis on diaphragmatic mechanics in man. patterns in patients with normal and poor left
Anesthesiology 1974; 41:242-255. ventricular reserve. Crit Care Med 1982; 10:423-6.
15. Westbrook PR, Stubbs SE, Sessler AD et al. Effects 33. Haldjen E, lakobsen S, laner L, NorJjen K. Effects of
of anesthesia and muscle paralysis on respiratory positive end-expiratory pressure on cardiac output
mechanics in normal man. 1 Appl Physiol 1973; distribution in the pig. Acta Anaesthesiol Scand 1982;
34:81-86. 26:403-8.
16. Rehder K, Went he FM, Sessler AD. Function of each 34. Hills BA. What forces keep the airspaces of the lungs
lung during mechanical ventilation with ZEEP and dry? Thorax 1982; 37:713-717.
with PEEP in man anaesthetized with thiopental- 35. Erdmann Al, Vaughan TR, Brigham KL, Woolverton
meperidine. Anesthesiology 1973; 39:597-606. WC, Staub NC. Effect of increased vascular pressure
17. Dery R, Pelletier 1, lacques A et al. Alveolar collapse on lung fluid balance in unanesthetised sheep. Circ
induced by denitrogenation. Canad Anaesth Soc 1 Res 1975; 37:271-84.
1965; 12:531-544. 36. Faridy EE, Permutt S, Riley RL. Effect of ventilation
18. Sutherland PW, Katsura T, Milic Emili 1. Previous on surface forces in excised dogs' lungs. 1 Appl
volume history of the lung and regional distribution of Physiol1966; 21:1453-1462.
gas. 1 Appl Physiol 1968; 25:566-574. 37. Webb M, Tierney D. Experimental pulmonary
19. Landmark Sl, Knopp Tl, Rehder K, Sessler AD. oedema due to intermittent positive pressure
Regional pulmonary perfusion and VIQ in awake and ventilation with high inflation pressures: protection by
anesthetised-paralysed man. 1 Appl Physiol 1977; positive end-expiratory pressure. Am Rev Resp D
43:993-1000. 1974; 110:556.
20. Dueck R, Wagner PD, West lB. Effect of positive 38. Bo G, Hauge A, Nicolaysen G. Alveolar pressure and
end-expiratory pressure on gas exchange in dogs with lung volume as determinants of net transvascular fluid
normal and edematous lungs. Anesthesiology 1977; filtration. 1 Appl Physiol 1977; 42:476-482.
47:359-366. 39. Russell lA, Hoeffel 1, Murray IF. Effect of different
levels of positive end expiratory pressure on lung
21. Fairley HB, Blenkarn GD. Effect on pulmonary gas water content. 1 App1 Physiol 1982; 53:9-15.
exchange of variations in inspiratory flow rate during 40. Demling RH, Staub NC, Edmunds LH lr. Effect of
intermittent positive pressure ventilation. Br 1 end expiratory airway pressure on accumulation of
Anaesth 1966; 38:320-328. extravascular lung water. 1 Appl Physiol 1975;
22. Macklin MT, Macklin Cc. Malignant interstitial 38:907-912.
emphysema of the lungs and mediastinum. Medicine 41. Hopewell PC, Murray IF. Effects of continuous
1944; 23:281-358. positive pressure ventilation in experimental
Anaesthesia and Intensive Care. Vol. 14, No. 3, August, 1986
 IPPV PHYSIOLOGY 235

pulmonary edema. J Appl Physiol 1976; 40:568-574. intracranial pressure in man. J Neurosurg 1977;
42. Fisher AB. Oxygen therapy: side effects and toxicity. 46:227-232.
CONF. Am Rev Resp D 1980; 122:61-69. 50. Weisman IM, Rinaldo JE, Rogers RM, Sanders MH.
43. Suter PM, Fairley HB, Isenberg MD. Optimum end- Intermittent Mandatory Ventilation. Am Rev Resp D
expiratory airway pressure in patients with acute 1983; 127:641-647.
pulmonary failure. N Engl J Med 1975; 292:284-289. 51. Bachrendtz S, Santesson J, Bindslev L, Hedenstierna
44. Bonnet F, Richard C, Glaser P et al. Changes in G, Matell G. Differential ventilation in acute bilateral
hepatic blood flow induced by continuous positive lung disease. Influence on gas exchange and central
pressure ventilation in critically ill patients. Crit Care haemodynamics. Acta Anaesthesiol Scand 1983;
med 1982; 10:703. 27:270-7.
45. Jarnburg PO, Dominguez de Villata E, Eklund J, 52. Hedley-White J, Laver MB, Bendixen MM. The effect
Granberg PO. Effects of positive end expiratory of changes in tidal volume on physiological shunting.
pressure on renal function. Acta Anaesthesiol Scand Am J Physiol 1964; 206:891.
1978; 22:508-514. 53. Sykes MK, Lumley 1. The effect of varying
46. Hall SV, Johnson EE, Hedley-White J. Renal inspiratory:expiratory ratios during anaesthesia for
hemodynamics and function with continuous positive open heart surgery. Br J Anaesth 1969; 41:374-80.
pressure ventilation in dogs. Anesthesiology 1974; 54. Grace MP, Greenbaum DM. Cardiac performance in
41 :452-461. response to PEEP in patients with cardiac
47. Hemmer M, Viquerat CE, Suter PM, Vallotton MB. dysfunction. Crit Care med 1982; 10:358.
Urinary antidiuretic hormone excretion during 55. Snyder JV, Carrol Gc. Tissue oxygenation: a
mechanical ventilation and weaning in man. physiologic approach to a clinical problem. Curr Prob
Anesthesiology 1980; 52:395-400. Surg 1982; 19, 11:649-719.
48. Hemmer M, Suter P. Treatment of cardiac and renal 56. Fairley HB. Critique of intermittent mandatory
effects of PEEP with dopamine in patients with acute ventilation. Int Anesth Clin 1980; 18, 2: 179-189.
respiratory failure. Anesthesiology 1979; 50:399-403. 57. Downs JB, Douglas ME. Intermittent mandatory
49. Apuzzo ML, Weiss MH, Petersons V et al. Effect of ventilation, why the controversy? Crit Care Med 1981;
positive end expiratory pressure ventilation on 9:622.

Anaesthesia and Intensive Care, Vol. 14, No. 3, August, 1986