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Pressure-controlled mechanical ventilation 

Pressure-controlled mechanical ventilation
Chapter:
Pressure-controlled mechanical ventilation
Author(s):

Thomas Muders

and Christian Putensen

DOI:
10.1093/med/9780199600830.003.0096
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date: 27 November 2020

Key points

  • Pressure-controlled, time-cycled ventilation (PCV) enables the physician to keep airway pressures under strict limits in order to minimize the risk for ventilator-associated lung injury in patients with acute respiratory distress syndrome.

  • During PCV inspiratory and expiratory pressures, and cycle times have to be chosen by the physician. These presets, as well as respiratory system mechanics determine (decelerating) inspiratory gas flow, tidal volume, and intrinsic positive end-expiratory pressure (PEEPi).

  • To avoid a harmful rise in tidal volume with improvement in respiratory system mechanics, continuous display, and tight monitoring of tidal volume is mandatory during PCV.

  • When compared with flow-controlled, time-cycled (‘volume-controlled’) ventilation, PCV reduces peak airway pressure, while mean airway, and mean alveolar pressures and gas exchange improve. However, no consistent data exist, showing PCV to improve patient outcome.

  • Airway pressure release ventilation (APRV) allows superimposed and unrestricted spontaneous breathing and, thereby, improves haemodynamics and gas exchange, whereas need for sedation, vasopressors and inotropic agents and duration of ventilator support decreases.

Introduction

Today’s lung protective ventilatory strategies reduce tidal volume (VT) to 6 mL/kg ideal body (iBW) [1]‌ and limit airway pressures [1] to minimize risk for ventilator associated lung injury (VALI) and to improve outcome in patients with acute respiratory distress syndrome (ARDS).

In contrast to flow-controlled, time-cycled ventilation (= ‘volume-controlled’, VCV) using a squared flow control, during pressure-controlled (preset), time-cycled ventilation (PCV) a preset square-wave pressure is applied to the airway. PCV results in a decelerating inspiratory gas flow holding the alveoli inflated for a preset period of time. In this chapter, we try to point out the principle and special characteristics, and physiological effects of pressure-controlled, time-cycled, continuous mandatory mechanical ventilation (PC-CMV), a prototype of PCV. Furthermore, we will discuss important variants of PCV, such as assisted PCV (PC-A/C), pressure-controlled inverse-ratio ventilation (PC-IRV) and pressure-controlled airway pressure release ventilation (PC-APRV).

Principle characteristics of PCV

PCV results in a square-wave pressure to the airway and a decelerating inspiratory gas flow holding the alveoli inflated for a preset period of time (Fig 96.1). Flow will initially enter the lung rapidly to reach the preset airway pressure as quickly as possible. As the open and fast-filling alveoli fill, and their pressure reaches equilibrium with the preset pressure, flow will decelerate, whereas slow compartments continue to fill with gas. The ventilator will constantly adjust gas flow so that inspiratory pressure is maintained during the entire set inspiratory time. Flow will continue until the preset pressure reaches equilibrium with alveolar pressure throughout all lung units, which is indicated by the flow pattern decelerating to zero [2]‌. During expiration, pressure is released abruptly, and the lung will passively deflate against the set PEEP level. VT depends mainly on respiratory compliance and resistance, and the difference between the preset pressure levels [2].

Fig. 96.1 Time (t) courses of airway pressure (Paw), flow 
(
V
˙
)
, and volume (V) during pressure-controlled (PCV) (left) and volume-controlled (VCV) (right) mechanical ventilation.

Fig. 96.1 Time (t) courses of airway pressure (Paw), flow ( V ˙ ) , and volume (V) during pressure-controlled (PCV) (left) and volume-controlled (VCV) (right) mechanical ventilation.

PINSP, inspiratory pressure; Pexp, expiratory pressure; Pmean, mean airway pressure; PIP, positive inspiratory pressure (= driving pressure); Ppeak, Peak inspiratory pressure; Pplat, plateau pressure; TINSP, inspiratory time; Texp, expiratory time. See text for details.

Input parameters of PCV

During PCV principally, inspiratory and expiratory pressures, and cycle times have to be chosen by the physician, but the way to determine these parameters depends on the ventilator.

Expiratory and inspiratory airway pressures

Apart from external positive end-expiratory pressure (PEEPe) driving pressure (positive inspiratory pressure, PIP) as pressure increment above PEEPe or absolute inspiratory pressure (PINSP) can be set (Fig. 1).

Ventilator rate, and expiratory and inspiratory time

Furthermore, ventilator rate (VR) and fractional inspiratory time (duty cycle, TINSP/TTOT) or VR, and inspiratory-to-expiratory ratio (I:E) has to be chosen. Alternatively, expiratory (TEXP) and inspiratory (TINSP) times can be set directly (Fig. 96.1).

Output parameters of PCV

Global and regional respiratory system mechanics (compliance and resistance) affect alveolar pressure (PA), intrinsic PEEP (PEEPi), inspiratory gas flow, VT, total minute and alveolar ventilation, resulting from preset airway pressures and cycle times.

Inspiratory flow

Depending on the respective ventilator, the abruptness of rise to peak flow can be modulated by setting slope or inspiratory rise-time. Rampant rise in flow might create some pressure overshoot that does not lead to elevated peak alveolar pressure and may not be associated with harm to the lung [3]‌. In contrast, longer rise-times creating a shallow increase to peak flow might be associated with a slow ramp of inspiratory pressure and have been reported to cause a delayed filling of the lung [4].

Mean airway pressure

Due to the squared waveform of the airway pressure during PCV, mean airway pressure ( P¯ aw , that is the is the integral of Paw over time divided by duration of a single breath (TTOT) can easily be calculated as

P¯ aw = ( PEEP e × T EXP + P INSP × T INSP ) / T TOT
[eqn 1]

Thus, during PCV changes in P¯ aw can directly be predicted from variations in preset airway pressures or cycle times. P¯ aw increases with increasing PEEPe, PINSP or I:E, whereas it decreases with decreasing PEEPe, PINSP or I:E (Fig 96.1). In contrast, changes in frequency maintaining I:E constant do not affect P¯ aw .

Alveolar pressure

During PCV PA can never exceed preset PINSP . Mean alveolar pressure ( P¯ A ) is closely related to mean airway pressure ( P¯ aw ) and affected by minute ventilation (VE) and inspiratory (RI) and expiratory (RE) resistances [3]‌:

P¯ A = P¯ aw + V E × ( R E R I )
[eqn 2]

If inspiratory and expiratory resistances are similar, changes in VR do not relevantly influence P¯ aw . When RE exceeds RI, P¯ aw relevantly underestimates P¯ A , and increments in VR may cause a noteless increase in P¯ A . This phenomenon is pronounced when VE is high and common in chronic obstructive lung diseases [3]‌. Peak PA equilibrates to Paw at end-inspiration when a sufficient inspiratory time is provided. With increasing VR and/or decreasing TINSP peak, PA falls below PINSP, whereas end-expiratory PA rises above PEEPe with increasing VR and/or decreasing TEXP [3] creating PEEPi (Fig 96.2).

Fig. 96.2 Time courses of airway pressure (Paw), volume (V), and flow (
                (
               
                V
                ˙
                
                )
    ) during pressure controlled ventilation. Shortening inspiration (red arrow and area) can cause incomplete regional filling and persisting end-inspiratory flow. Shortening expiration (blue arrow and area) can cause intrinsic PEEP, regional air trapping, and persisting end-expiratory flow. See text for detailed influence of I:E ratio, inverse ratio, and respiratory frequency.

Fig. 96.2 Time courses of airway pressure (Paw), volume (V), and flow ( ( V ˙ ) ) during pressure controlled ventilation. Shortening inspiration (red arrow and area) can cause incomplete regional filling and persisting end-inspiratory flow. Shortening expiration (blue arrow and area) can cause intrinsic PEEP, regional air trapping, and persisting end-expiratory flow. See text for detailed influence of I:E ratio, inverse ratio, and respiratory frequency.

Intrinsic PEEP

PEEPi occurs when regional or total expiration remains incomplete within the TEXP available leading to dynamic hyperinflation [5]‌. This dynamic phenomenon depends on a complex function of the respiratory mechanics and the input parameters of PCV [6].

PEEPi can be increased either by higher driving pressure (resulting in higher VT during PCV), higher I:E ratio or higher VR (both shortening TEXP). As described previously and in Fig. 96.2, changes in PA are mainly affected by differences between RI and RE. Thus, increasing I:E ratio might elevate PEEPi up to maximal airway pressure, whereas pure increases in VR will reduce peak PA and increase PEEPi [3]‌.

Furthermore, higher respiratory time constants increase PEEPi for the same input parameters [5]‌. As the time constant (t) is equal to resistance (R) × compliance (C), high time constants are caused by high airway R and/or C, which may occur on a regional basis, e.g. in slow compartments, as well as for the whole respiratory system [7]. It is important to note that elevation in airway resistance also can be caused by the design of the ventilator circuit (e.g. narrow tubes, slow PEEP valves) [7].

In inhomogeneous lungs different PEEPi may occur [8]‌ and mainly the slower compartments will profit from PEEPi in terms of alveolar recruitment, whereas fast compartments might be overinflated (Fig 96.2).

Tidal volume

In contrast to VCV, which ensures a preset VT, during PCV VT mainly depends on the difference between the preset pressure levels, VR or cycle times, and respiratory compliance and resistance. To enable a nearly-complete lung inflation TINSP should be longer than three times the time constants of the respiratory system, leading to a minimal TINSP of 1.0–1.5 s in healthy intubated adults. In obstructive patients, this time can rise to 2–4 s, whereas in patients suffering from ARDS, lung can be inflated within 0.8–1 s due to reduction in lung compliance [3]‌. Furthermore, incomplete lung emptying will decrease VT. Therefore, TEXP should be longer than three expiratory time constants. Hence, incomplete lung filling will occur with VR above 25–30 breaths/min. Generally, during PCV increasing I:E ratio mainly increases PEEPi, whereas reductions in VR cause reduced peak PA and increased PEEPi, and thereby further decrease effective driving pressure. Thus, VT is more affected by changes in VR than by altered I:E ratio (Fig 96.2).

At this point it is important to note, that VT will change with changes in lung mechanics. When the lung is recovering over time and lung compliance improves, VT will rise and may relevantly exceed the limits of lung protective ventilation. In this situation, inspiratory pressure has to be reduced to keep VT below 6 mL/kg iBW. Therefore, respiratory mechanics and VT have to be carefully monitored during PCV.

Alveolar and minute ventilation

As long as complete lung filling and emptying is ensured, increasing VR will improve total minute and alveolar ventilation, and thereby CO2 elimination. At higher VR and decreases in TINSP, peak PA will not equilibrate to preset inspiratory pressure causing incomplete filling of slow lung compartments and a decline in VT. As a consequence, functional dead space to tidal volume ratio will increase, and CO2 elimination will be impaired by decreased alveolar ventilation. In clinical practice, with a fixed non-inverse I:E ratio, VR can be increased to improve CO2 elimination until VT decreases by 25–30%. A further increase in VR will be counterproductive due to increased dead space, even when VE increases [3]‌.

Physiological effects of PCV

The effects of using PCV when compared with VCV, while keeping all other parameters (VR, I:E ratio, PEEP and plateau pressure) constant can be summarized as follows.

Airway and alveolar pressures

During PCV decelerating flow reduces peak Paw, but increases mean Paw [9]‌. Homogeneity of regional peak PA distribution within the lung is improved with PCV, reducing exposure of more diseased lung units to high pressures.

Ventilation distribution and pulmonary gas exchange

PCV seems to favour ventilation of slow lung units due to fast gas flow during early inspiration. As a consequence, PaCO2 falls, since dead space ventilation is decreased, whereas arterial oxygenation is slightly improved [9]‌. However, clinical relevance of PCV-related advantages remains debatable.

Cardiovascular effects

The application of positive pressure ventilation generates an increase in airway and, therefore, in intrathoracic pressure, which in turn reduces venous return to the heart. This produces a reduction in right- and left-ventricular filling, and results in decreased stroke volume, cardiac output, and oxygen delivery [10]. For comparable mean airway pressures no differences in haemodynamic impairment were seen between PCV and VCV. Since influence of changes in ventilator settings on P¯ aw is more predictable with PCV, haemodynamic impairment should also be more predictable.

Ventilator-associated lung injury

Regional lung strain calculated from computed tomography scans is comparable between PCV and VCV [11]. Although, experimental data suggest PCV to reduce VALI, no consistent results have been seen with respect to reduced barotrauma or improved outcome in patients [12].

Variants of PCV

Assisted PCV

Assisted PCV (PC-A/C) enables the patient to trigger the ventilator and in opposite to pressure-support ventilation (PSV) time and not flow determines the cycle off. Compared with PSV, a risk of prolongation of TINSP by not reaching the default expiratory triggering threshold (e.g. mask leaking, severe obstruction), and resulting insufficient drop in inspiratory flow is lower under assisted PCV [3]‌. Therefore, TINSP must be adjusted to match the patient’s spontaneous TINSP, usually 0.6–1.2 seconds [13]. This gives more security for the patients, but also avoids freedom of ventilation pattern (restraining, for instance, the possibility of a spontaneous sigh and potentially increasing discomfort) [13].

With assisted PCV, breaths are triggered either by the patient’s effort or by elapsed expiratory time, guaranteeing lower central apnoeas and sleep fragmentation. When compared with assisted VCV (flow-controlled, volume-cycled), assisted PCV results in lower peak Paw and reduced workload [3]‌.

Pressure-controlled inverse ratio ventilation

In healthy patients breathing for themselves, the ratio of the time spent in inspiration to that in expiration is about 1:2. Therefore, traditionally, the I:E ratio has been usually set at 1:2 or 1:1.5 to approximate the normal physiology. In inverse ratio ventilation (IRV) the TINSP is prolonged (I:E ratio is inversed), thereby increasing P¯ aw and allowing the use of lower Paw limits. This alternative ventilation strategy was initially developed to treat infants and adopted for adult patients with ARDS the early 1980s to improve severe hypoxaemia [8]‌. IRV can be delivered using pressure controlled, time-cycled ventilation (PC-IRV) [9] or flow-controlled (‘volume-controlled’), time-cycled ventilation (VC-IRV) [8].

Principle of PC-IRV

The effects of changes in TINSP and I:E ratio on Paw and PA can be summarized thus: the elongation of inspiratory time increases P¯ aw , enables equilibration of peak PA to preset PINSP, and causes full lung inflation of even slow lung compartments. Shortening TEXP leads to incomplete lung emptying and causes an increase in PEEPi [8,9]. Both mechanisms increase P¯ A and thereby transpulmonary pressure that is the driving force to recruit non-aerated alveoli and to prevent alveolar recollapse during expiration. This reduces intrapulmonary shunting and improves arterial oxygenation. Therefore, during IRV elevation in P¯ aw is a major determinant of improved oxygenation [5,14].

Physiological effects of PC-IRV

When compared with conventional mechanical ventilation using an increased PEEPe to reach the same magnitude of PEEPTOT as that produced intrinsically by IRV (PEEPTOT = PEEPe + PEEPi), IRV had no advantage [15]. Furthermore, CT observations in experimentally-induced lung injury showed no improvement in lung aeration, but demonstrated that during IRV the upper, already well-aerated lung regions become even more aerated, whereas poorly- or non-aerated lung units localized in the dependent lung regions are less aerated when compared with conventional mechanical ventilation with essentially the same mean airway pressure and extrinsic/intrinsic PEEP [16].

A major problem during IRV is that PEEPi changes, due to altered respiratory mechanics for example, may not be immediately clinically evident. A remaining terminal flow at the end of the expiration indicates that a certain PEEPi exists, but it does not quantify the amount [8]‌. Therefore, careful monitoring and continuous display of VT and expiratory flow has to be recommended during PC-IRV.

Limitation of PC-IRV

The long TINSP of usually makes IRV incompatible with spontaneous breathing, and respiratory depressants or muscle relaxants must be administered to assure patient acceptance. Deep sedation sufficient to suppress respiratory efforts is known to cause significant cardiovascular depression [17]. Incompatibility with spontaneous breathing is a major limitation of IRV.

Airway pressure release ventilation (APRV)

APRV incorporates the characteristics of PCV, PC-IRV, spontaneous breathing, and partial ventilatory support into one technique with potentially widespread applicability. Based on the clinical and experimental data, APRV is indicated in patients with ARDS, and atelectasis after major surgery.

Principles of APRV

APRV provides a squared pressure pattern identical to PCV by time-cycled switches between two pressure levels in a high flow or demand valve continuous positive airway pressure (CPAP) circuit, while allowing unrestricted and unsupported spontaneous breathing in any phase of the ventilator cycle (Fig 96.3) [17,18].

Fig. 96.3 Time courses of airway pressure (Paw) biphasic-positive-airway-pressure (BIPAP) airway-pressure-release-ventilation (APRV). Both modes similarly provide a time-cycled switch between two different airway pressures and allow unrestricted spontaneous breathing at any time point and pressure. In the absence of spontaneous breathing BIPAP and APRV are equal to PCV. See text for details.

Fig. 96.3 Time courses of airway pressure (Paw) biphasic-positive-airway-pressure (BIPAP) airway-pressure-release-ventilation (APRV). Both modes similarly provide a time-cycled switch between two different airway pressures and allow unrestricted spontaneous breathing at any time point and pressure. In the absence of spontaneous breathing BIPAP and APRV are equal to PCV. See text for details.

The degree of ventilator support with APRV is determined by the duration of the two CPAP levels and the mechanically delivered VT [17,18]. VT depends mainly on respiratory compliance and the difference between the CPAP levels. By design, changes in ventilatory demand do not alter the level of mechanical support during APRV. When spontaneous breathing is absent, APRV is not different from conventional PCV [17,18].

Synonyms used for APRV are biphasic positive airway pressure (BIPAP) [17] and bi-level airway pressure (Bilevel). BIPAP is identical to APRV except that no restriction is imposed on the duration of the low CPAP-level (release pressure) [17,18]. Based on the initial description, APRV keeps the duration of the low CPAP-level (release time) at 1.5 seconds or less (Fig 96.3).

Physiological effects of superimposed spontaneous breathing during APRV

As known from CT scans in patients with ARDS, alveolar collapse is primarily localized in the dependent lung regions (Fig 96.4), which correlates with intrapulmonary shunting and accounts entirely for the observed hypoxaemia [19]. If the diaphragm is relaxed, it will be moved by the weight of the abdominal cavity and intra-abdominal pressure towards the cranium. During spontaneous breathing, the posterior muscular sections of the diaphragm moves more than the anterior tendon plate [17]. Thereby, transpulmonary pressure will be increased especially in dependent lung regions. Periodic reduction of intrathoracic pressure, achieved by maintaining spontaneous breathing, promotes venous return to the heart and right- and left-ventricular filling and improves outflow from the right ventricle (the major determinant of pulmonary vascular resistance), thereby increasing cardiac output and oxygen delivery [17].

Fig. 96.4 Densitometric analysis of computed tomography scans (pig, experimental lung injury) during BIPAP/APRV with (orange) and without (blue) spontaneous breathing. Spontaneous breathing increase end-expiratory lung volume, decreases atelectasis and redistributed regional ventilation into dependent lung regions.

Fig. 96.4 Densitometric analysis of computed tomography scans (pig, experimental lung injury) during BIPAP/APRV with (orange) and without (blue) spontaneous breathing. Spontaneous breathing increase end-expiratory lung volume, decreases atelectasis and redistributed regional ventilation into dependent lung regions.

Data from Wrigge H et al., ‘Spontaneous breathing with airway pressure release ventilation favors ventilation in dependent lung regions and counters cyclic alveolar collapse in oleic-acid-induced lung injury: a randomized controlled computed tomography trial’, Critical Care, 2005, 9(6), pp. R780–9.

In clinical and experimental studies spontaneous breathing with APRV in is associated with recruitment of atelectasis and increased end-expiratory lung volume (Fig 96.4) [20], improved ventilation of dependent lung areas, and thereby improved ventilation–perfusion matching, a rise in cardiac output, oxygenation and oxygen delivery [17], whereas oxygen consumption remains unchanged despite the work of spontaneous breathing. Furthermore, tidal recruitment (cyclic collapse) that might be a major contributor to VALI is reduced [20] . Renal, intestinal, and cerebral perfusion have been shown to be increased [17].

When allowing spontaneous breathing, lower levels of sedation are possible. Less sedation helps in reducing the doses of vasopressor and inotropic agents, while maintaining cardiovascular function in a stable condition, and reducing the duration of ventilator support [17].

Limitations for APRV

In patients with left ventricular dysfunction, switching abruptly from controlled to supported ventilation with a simultaneous reduction in airway pressure might cause further decompensation due to augmentation right ventricular preload and increase in left ventricular afterload. Provided that satisfactory CPAP levels are applied, maintaining spontaneous breathing during APRV should not be a disadvantage and is not per se contraindicated in patients with ventricular dysfunction.

In concept, APRV does not provide breath-to-breath assistance of spontaneous inspiration. Thus, APRV is not expected to be an advantage in difficult-to-wean patients.

Because lower levels of sedation are used to allow spontaneous breathing, APRV should not be used in patients who require deep sedation for management of their underlying disease (e.g. cerebral oedema with increased intracranial pressure).

Acknowledgements

The authors would like to thank Stefan Kreyer, MD, DESA, staff anaesthesiologist at the Department of Anesthesiology and Intensive Care Medicine, University of Bonn, Germany, for his important input and support.

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