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Setting rate, volume, and time in ventilatory support 

Setting rate, volume, and time in ventilatory support
Chapter:
Setting rate, volume, and time in ventilatory support
Author(s):

Charles M. Oliver

and S. Ramani Moonesinghe

DOI:
10.1093/med/9780199600830.003.0093
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date: 19 October 2020

Key points

  • Ventilator rate, volume, and time parameters are interrelated directly, mechanically, and physiologically.

  • The physiological consequences of mechanical ventilation and risks of ventilator-induced trauma may be exacerbated by lung pathology.

  • Programming of parameters should be considered within the context of an individualized ventilation strategy to achieve adequate gas exchange, while minimizing attendant risks of mechanical ventilation.

  • Recommended strategies should be modified within accepted limits to mitigate disease-specific risks.

  • Parameters should subsequently be titrated against blood gas- and ventilator-derived targets and other clinical variables.

Introduction

While mechanical ventilation (MV) remains a cornerstone of critical care practice, understanding of its optimal usage continues to evolve. Striving for proposed physiological ideals has given way to strategies targeting more modest PaO2, PaCO2, and pH values, thereby reducing risks of volutrauma, barotrauma, atelectrauma, and bio-trauma, which may exacerbate or perpetuate lung injury [1,2].

Interactions between intrinsic pulmonary physiomechanics, pathological processes, and the effects of positive pressure ventilation are complex. Programming of ventilator parameters must therefore be considered within the context of an individualized ventilation strategy in order to achieve gas exchange targets, while minimizing the attendant risks of MV.

Rate, volume, and time

Rate, volume, and time parameters are interrelated directly, physiologically, and mechanically.

Minute ventilation (min) is the gas flow per minute, which is calculated as the product of the inspiratory volume, or tidal volume (VT) and the ventilatory rate. VT and rate are readily amenable to manipulation, and may be titrated to biochemical and physiological targets in MV.

Programming of absolute duration of inspiratory and expiratory phases of ventilation, and their ratio is necessarily limited by ventilatory rate. Furthermore, setting inspiratory time in volume-targeted modes may limit the magnitude of delivered gas flow and result in excessive system pressures. Disease-specific factors must be considered when setting expiratory time.

MV may be broadly classified as mandatory, assisted, or a combination. Rate, volume, and time values must be selected in mandatory modes, although this may be performed automatically. Spontaneous inspiration is augmented to a target pressure or volume in assisted modes and a back-up rate may be set to provide additional ventilator-delivered breaths. The duration of inspiration and expiration may be programmed in both mandatory and assisted modes.

Rate

In conventional mandatory ventilation a rate of 10–20 breaths/min will usually provide a min sufficient to create and maintain favourable partial pressure gradients across alveolar membranes. Higher rates may be indicated in certain disease states and are routinely selected for children, infants, and neonates. Rates in excess of three times the physiological range are used in high frequency ventilation, and lower rates may be programmed for ventilator weaning and in individuals susceptible to gas-trapping.

Provided VT remains constant, increasing ventilatory rate will increase alveolar ventilation, which may be beneficial. However, in addition to its additive role in ventilator-induced lung injury (VILI) [3]‌, increasing ventilatory rate limits inspiratory and expiratory times, which may worsen gas exchange and predispose to complications in susceptible individuals as discussed in ‘Targets in Pathophysiological States’.

Volume

Of the generated inspiratory volume (VT), a proportion is unavailable for gas exchange. This ‘dead space’ volume comprises physiological (conducting airways and alveoli at which no gas exchange occurs) and apparatus dead space. While the former is relatively fixed, the latter should be minimized to optimize ventilatory efficiency. The flow of fresh gas (A) available for exchange in the alveolar compartment is therefore the product of ventilatory rate and what remains of VT once dead space volume is accounted for:

V ˜ A   =   r . [ V T     ( V D   + V A P P ) ]
[eqn 1]

where A is alveolar ventilation, r is rate, VT is tidal volume, VD is physiological dead space volume, and VAPP, apparatus dead space volume.

Provided alveolar perfusion matches ventilation, oxygenation and CO2 elimination may be improved by increasing alveolar ventilation relative to dead space ventilation. It should, however, be noted that simply increasing rate will lead to a proportionally greater increase in dead space ventilation relative to A.

Tidal volume may be increased in positive pressure ventilation (PPV) by increasing generated inspiratory pressure with due attention to rate and time variables; however, the volume delivered is also dependent upon system compliance. Pathological processes resulting in differential regional compliance may cause asymmetrical distribution of gas flow and pressure inequalities in affected individuals. Such changes predispose to dynamic hyperinflation, over-distension of alveoli in more compliant lung units and exaggeration of physiological gas flow:perfusion (A:Q) mismatching.

Evidence of the potential harm caused by exposure to MV comes from studies of the pathogenesis of VILI and the acute respiratory distress syndrome (ARDS). While the aetiology of ARDS is likely to involve synergy between pulmonary insult and MV in predisposed individuals [4,5], VILI may develop in previously normal lungs in as little as 6hours [4,6,7]. Demonstrated associations include exposure to high end-inspiratory lung volumes (volutrauma) [8]‌, shear stress resulting from cyclical inflation and deflation of differently compliant lung units (atelectrauma), and large transpulmonary pressure gradients [9].

Data from ARDS trials suggest that limitation of VT to 4–8 mL/kg ideal body weight (IBW) [10,11] and limitation of plateau pressure (a surrogate for transpulmonary pressure) to less than 30–35 cmH2O [10] may decrease early morbidity and mortality in affected individuals. However, due to increasing evidence of the potentially deleterious effects of high inflationary pressures and inspiratory volumes, such lung protective strategies are increasingly being adopted in the management of patients with previously normal lungs [12]. Targets include VT 6–8 mL/kg IBW [13,14] and limitation of plateau pressure (PPLAT) to 30 cmH2O [12].

As can be seen from eqn 1, the limitation of VT and PPLAT without compensatory increase in rate may result in hypercapnoea in poorly compliant lungs. It may therefore be necessary to accept supraphysiological PaCO2 or institute an alternative means of CO2 removal.

Additional strategies to aid improved ventilation include the manipulation of time, rate, and mode variables to limit airway pressures and improve flow distribution, titration of positive end expiratory pressure (PEEP) to limit atelectrauma [15] and shunt, patient repositioning, and pharmacological agents.

Time variables

Time variables, which may be individually programmed or automatically determined include duration of inspiration and expiration and their ratio (I:E ratio). These variables are interdependent and limited by ventilatory rate; furthermore, their manipulation may predispose to complications.

To permit theoretical modelling, groups of alveoli and their terminal airways possessing similar mechanical characteristics are termed ‘lung units’. The time required to fully inflate or deflate such units is determined by both compliance and resistance to flow, the product of which, the time constant (τ‎), determines the speed with which alveolar and proximal airway pressures reach equilibrium.

Many disease processes affect lung tissue mechanics and thus inspiratory (τ‎i) and expiratory (τ‎e) time constants, but because such changes are rarely homogenous, regional flow pattern variations occur. Lung units with low τ‎i tend to fill quickly with a subsequent distribution of flow to more distensible units with greater resistance. PPV may therefore cause over-distension of compliant units and subsequent collapse of compressed units in a variety of pathologies, predisposing to complications and exaggerating A:Q mismatching.

Time variables may be controlled in both mandatory and assisted modes of ventilation; however, it is imperative to ensure synchrony with spontaneous effort to reduce distress, work of breathing, and breath stacking. Time variables must therefore be considered both individually and as components of an individualized strategy.

Inspiratory time

Inspiratory time (ti) is the duration over which pressure is applied in PPV to deliver VT and is typically set at 1 second when respiratory rate is 20 breaths/minute. Any increase in ti occurs at the expense of expiratory time (te), unless rate is reduced to compensate.

Increasing ti may improve oxygenation by permitting equilibration of pressure between differently compliant lung regions, increasing mean airway pressures, and preventing atelectasis. Reducing ti predisposes to the complications of increased flow and system pressures in volume-controlled modes [8]‌.

Expiratory time

Expiratory time (te) is typically set at 2 seconds when rate is 20 breaths/minute, and may only be maintained or increased at the expense of ti at higher rates.

Pressures generated in PPV may be sufficient to overcome increased airway resistance and distend alveoli, but exhalation is passive and diminished if tissue elasticity is reduced. Conditions in which highly compliant alveoli empty into bronchioles with increased resistance to flow, such as chronic obstructive pulmonary disease (COPD), therefore require a longer te to permit lung unit emptying. If te is insufficient to permit emptying prior to inspiratory cycling, gas trapping and the generation of intrinsic PEEP (PEEPi) may occur, with both respiratory and haemodynamic consequences.

I:E ratio

This is usually set at 1:1 to 1:2, but ratios of 1:2 to 1:4 may be required to prevent dynamic hyperinflation in severe airflow limitation. Awake patients may be more comfortable with shorter inspiratory times and high inspiratory flow rates.

Inverse ratio ventilation (IRV), in which ti exceeds te, may be employed if adequate oxygenation cannot be achieved by increasing PEEP. It is thought that increased mean airway pressures and improved filling of lung units with high τ‎i are responsible for its effects. Caution should be exercised in using IRV in patients with airflow limitation to avoid generation of PEEPi.

Proposed benefits of IRV include:

  • Reduced shunt due to prevention and resolution of atelectasis.

  • Increased efficiency of CO2 elimination due to delayed lung unit emptying.

  • Lower VT and transpulmonary pressures due to reduced min.

Suggested strategy

  • Following a thorough clinical assessment, consider first whether lung physiomechanics are likely to be normal.

  • Targets in the absence of overt pulmonary pathology are shown in Table 93.1.

  • Adjust parameters in response to clinical examination, blood gas analysis, and monitoring. Recruitment manoeuvres may be required, particularly if a period of hypoventilation precedes institution of MV.

Table 93.1 Targets in the absence of overt pulmonary pathology

Rate

10–20 breaths/min

VT

6–8 mL/kg IBW

I:E

1:2

PPLAT

<30 cmH2O

PaO2 may be optimized by adjusting min, I:E ratio, PEEP, and FiO2. Normocapnoea should not be pursued at the expense of exceeding pressure limits, unless there is urgent indication to do so. Development of a respiratory acidosis (pH < 7.25) should prompt reconsideration of pathology, mode of ventilation, and alternative methods of CO2 removal.

Targets in pathophysiological states

Modify the parameters shown in the previous section considering predominant manifestations of pulmonary disease.

Airflow limitation

Narrowing of medium- and small-calibre airways significantly increases resistance to gas flow, disrupting regional and global pressure-flow relationships, and variably increasing time constants. Injudicious PPV programming in such individuals may result in volume redistribution, alveolar over-distension, and ventilator trauma.

Dynamic hyperinflation due to insufficient te and unfavourable I:E ratios exacerbates A/Q mismatching, and further increases the risk of trauma. PEEPi estimation may be necessary to avoid acute deterioration.

Restrictive lung disease

In the absence of significant airflow limitation, low compliance results in reduced τ‎. Affected lung units fill quickly, with rapid gas flow redistribution, A/Q mismatching and over-distension of relatively unaffected units. Attention to volume and pressure settings may mitigate risk of trauma in such individuals.

Emphysema

The characteristic destruction of lung parenchyma and diminishment of elastic recoil results in markedly increased compliance of affected tissue. Because tissue damage is patchy, with changes characteristic of causative agents and disease processes, affected units are slow to open and prone to over-distension. A low rate with long ti and te should be set to permit filling and emptying of slower units, and PPLAT limited to prevent trauma.

Copd

Because emphysematous changes co-exist with airflow limitation in COPD, both τ‎i and τ‎e may be significantly prolonged. A low rate and prolonged expiratory phase (I:E ratio 1:2.5 or 3.0) may allow for slow changes in airway flows and prevent gas trapping. Airway pressures must be limited to prevent over-distention and the potential for rupture of bullae.

Ards

ARDS is characterized by absolute volume loss with decreased total system compliance [16], but pathological changes are not evenly distributed and even targeting tidal volumes of 6–8 mL/kg may over-distend aerated lung units and exacerbate shunt through compression atelectasis.

Optimal ventilatory strategies in ALI and ARDS remain the subject of debate, with some advocating bedside quantification of injured and healthy lung volumes in order to permit individualization of VT targets and the limitation of regional distending pressures [17]. The weight of evidence supports limitation of VT to 4–8 mL/kg IBW [10,11] and plateau pressure to less than 30–35 cmH2O [10] as the least deleterious strategy.

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