JICS education: mechanical ventilation – physiology, mechanism and modes

Abstract

Mechanical ventilation remains a cornerstone of organ support in critically ill patients, yet modern intensive care ventilators incorporate increasingly complex modes and proprietary terminology that can obscure the physiological principles underpinning their use. A clear understanding of these principles is essential to enable safe, individualised, and lung protective ventilation. This article provides the physiological foundation for a four-part educational series on mechanical ventilation in adult critical care. Key concepts including positive end-expiratory pressure, airway pressures, resistance, compliance, elastance, and respiratory time constants are reviewed. Evidence supporting contemporary ventilation strategies is summarised, emphasising the importance of low tidal volume ventilation and individualisation of ventilator settings according to patient physiology. The ventilator breath cycle is described in terms of triggering, delivery, cycling, and expiration, providing a framework that is independent of manufacturer-specific nomenclature. A structured approach to ventilator modes based on control variables, breath sequence, and targeting schemes is presented using the Taxonomic Attribute Grouping system. Conventional pressure- and volume-controlled modes are discussed alongside assisted and mandatory ventilation strategies. Advanced modes, including airway pressure release ventilation and closed-loop systems, are reviewed with reference to their physiological rationale and current evidence base. Mechanical ventilation should be understood as a set of physiological principles rather than a collection of proprietary mode names. By focusing on pressure, flow, volume, timing, and patient–ventilator interaction, clinicians can better adapt ventilatory support to the changing pathophysiology of individual patients. This article aims to provide a practical framework for trainees and clinicians seeking to understand contemporary mechanical ventilation and to support subsequent articles addressing lung-protective ventilation, difficult weaning, and extracorporeal respiratory support.

Mapped Curriculum: ○ FICM curriculum – Domain 4: “Initiate, manage, and wean patients from invasive and non-invasive ventilatory support” Learning Aims: By the end of the article, the reader should be able to: - Describe the fundamental concepts and principles of mechanical ventilaton. - Explain the ventilator breath cycle. - Compare major modes of ventilation, including their indications, advantages and limitations. - Apply standardised, brand-neutral nomenclapture when describing ventilator modes and settings

Introduction

Mechanical ventilation (MV) remains a cornerstone of organ support in the intensive care unit (ICU). Modern ventilators are increasingly sophisticated, combining conventional modes of breath delivery with advanced monitoring, automation, and proprietary mode labels that are often absent from formal training curricula.

This article provides the physiological foundation for a wider educational series on mechanical ventilation in critically ill adults. Mechanical ventilation is best viewed as a set of physiological principles rather than a collection of ventilator brand names. Safe practice requires an appreciation of pressure, flow, volume, timing, and patient–ventilator interaction, together with the ability to apply these concepts to an individual patient’s pathophysiology. The aim is to support gas exchange while minimising lung injury, preserving respiratory muscle function, and adapting ventilatory support to the patient’s needs.

This article is the first in a four-part series on mechanical ventilation in critical care:

1. Mechanical ventilation: physiology, mechanisms and modes

2. Ventilatory strategies in ARDS: avoiding injury and protecting the lung

3. Difficult weaning and extubation

4. V-V ECMO: indications, physiology, and practical application

Together, these articles provide a structured framework for understanding the initiation, delivery, optimisation, and escalation of respiratory support in critically ill adults.

Epidemiology

A substantial proportion of ICU patients receive invasive mechanical ventilation. UK national audit data suggest that around one third of admissions to adult general critical care involve mechanical ventilation (55,000 patients/year), and mechanically ventilated patients have longer ICU stays than those who do not require ventilatory support. ¹ Respiratory failure remains one of the commonest indications for ICU admission, usually in the context of pneumonia, sepsis, acute respiratory distress syndrome (ARDS,) postoperative complications, or impaired airway protection. ²

Initiation of mechanical ventilation

The timing of intubation in acute respiratory failure remains controversial. No single threshold has been shown to define the optimal point for transition from non-invasive or less invasive support, to invasive ventilation. Decisions should therefore be individualised and based on the trajectory of illness, gas exchange, work of breathing, mental status, haemodynamic status, and response to preceding therapies. Current sepsis guidance emphasises ongoing clinical reassessment rather than a fixed trigger for intubation. ³ Although delayed intubation has been associated in some observational studies with worse outcomes, these data are vulnerable to confounding by indication and illness severity, and do not support a simple universal early-versus-late rule.^4–6

The ventilator breath cycle

Each ventilator breath can be understood by considering four phases: initiation, delivery, cycling, and expiration. ⁷ This framework is useful because it describes what the ventilator does in physiological terms, irrespective of the manufacturer’s trade name for a given mode (Figure 1).

Figure 1.

The ventilator breath cycle. (1) Initiation: Breaths may be mandatory, patient-triggered, or adaptive. (2) Delivery The ventilator delivers either a set pressure or a set flow. Pressure and flow profiles may be modified to optimise respiratory mechanics and minimise mechanical stress. (3) Cycling: Cycling may be time-based, volume-based (on reaching a preset tidal volume), or flow-based (when inspiratory flow falls to a set proportion of peak flow, reflecting a reduced pressure gradient). (4) Expiration: Usually passive, driven by elastic recoil, with gas expelled against airway resistance and PEEP. Flow-controlled or assisted expiration may be used to regulate expiratory mechanics. Overview of ventilator function. Figure created using Figure Lab software, with subsequent author modification.

Initiation

Breath initiation may be triggered by the ventilator (time-cycled) or by the patient. Patient triggering may occur through changes in pressure or flow, or via an electrical signal generated by diaphragmatic activation, as in neurally adjusted ventilatory assisted (NAVA). These mechanisms may also be combined within adaptive ventilation systems.

In assisted ventilation, the trigger must be sensitive enough to detect inspiratory effort but not to sensitive to detect non-respiratory signals that can cause auto-triggering. An insensitive trigger increases the work of breathing and may worsen patient-ventilator asynchrony. Conversely, an overly sensitive trigger may result in false triggering caused by leaks, cardiac oscillations, or circuit artefact.

Delivery

Delivery refers to the inspiratory phase of the breath cycle, during which the ventilator delivers gas to the patient. The ventilator controls either a pressure target or a volume target. In volume-controlled ventilation, the ventilator targets a set flow pattern to deliver the desired tidal volume, while airway pressure varies according to respiratory mechanics. In pressure-controlled ventilation, inspiratory pressure and inspiratory time are set, while flow and tidal volume vary according to patient effort and respiratory mechanics.

Flow delivery differs between modes. In volume-controlled ventilation, the inspiratory flow pattern may be selected by the clinician and can be constant, decelerating, or follow another predefined waveform depending on the ventilator. In pressure-controlled ventilation, flow is not directly set. Instead, flow is typically highest at the start of inspiration and then decelerates as the pressure target is reached. The rise time (or pressure ramp) determines how quickly the pressure target is achieved and influences patient comfort, patient-ventilator synchrony, and the resulting pressure and flow waveforms.

Cycling

Cycling refers to the mechanism that terminates inspiration. Depending on the mode, inspiration may end when a preset time has elapsed (time-cycled), when a target volume has been delivered (volume-cycled), or when inspiratory flow falls to a defined proportion of its peak value (usually 25%, but can be modified), as in pressure-support ventilation.

Expiration

Expiration during controlled ventilation is usually passive and driven by elastic recoil of the respiratory system. Its duration is determined indirectly by respiratory rate and inspiratory time. In patients with airflow limitation or long time-constants, insufficient expiratory time may cause gas trapping and intrinsic PEEP. Emerging technologies such as flow-controlled expiration modify expiratory flow more actively, with the aim of reducing derecruitment and improving the distribution of lung stress, but these approaches are not yet standard ICU practice. Flow-controlled ventilation (FCV), expiratory ventilation assistance (EVA), or flow-controlled expiration (FLEX) – actively regulate expiratory flow to make the process more gradual and lung-protective. These advanced modes decouple expiration from being purely passive, instead managing it with carefully controlled flow, often using flow-cycling thresholds to determine when expiration ends, analogous to the way an anaesthetist might gradually release pressure by adjusting an Adjustable Pressure Limiting (APL) valve during manual ventilation. The goal is to minimise airway collapse, maintain alveolar stability, and reduce ventilator-induced lung injury by controlling both phases of the breath. It is worth noting that this is advanced, rarely used and not expected knowledge within the curriculum.

Key terms and concepts

Positive-pressure ventilation is non-physiological and can have important mechanical, haemodynamic, and biological consequences. Understanding the core physiological principles of mechanical ventilation is therefore essential before ventilator settings are applied at the bedside.

Positive end-expiratory pressure (PEEP)

In mechanically ventilated patients, dependent lung regions and small airways are prone to collapse because of reduced respiratory muscle tone, sedation, increased superimposed weight, and pressure resulting from supine positioning. Depending on the severity of the underlying disease, alveoli can be either be collapsed and gasless (i.e. atelectatic, with loss of total lung volume), or gasless but filled with liquid or cellular or material (i.e. consolidated, where the total lung volume is maintained but the ventilated lung volume, in other words the volume of the lung that contains gas, is more or less significantly reduced).

Positive end-expiratory pressure (PEEP) is applied to counterbalance the forces leading to collapse of the alveoli and therefore it maintains end-expiratory alveolar volume, increases functional residual capacity, improves oxygenation, and when appropriately set, reduces cyclic tidal alveolar opening (recruitment) and collapse. This latter phenomenon leading to a modality of lung injury named atelectotrauma.

PEEP, which is generally set on the ventilator and measured at the airway opening, is based on oxygenation or titrated to achieve the best respiratory system compliance. However, end-expiratory alveolar pressure may be higher than the applied PEEP when expiratory flow limitation, dynamic hyperinflation, or short expiratory times lead to gas trapping. This additional pressure is named ‘intrinsic PEEP’, or auto-PEEP. Total PEEP is therefore the sum of extrinsic (i.e. externally set by clinicians on the ventilator) and intrinsic PEEP.

$$\mathrm{Total}\mathrm{PEEP}=\mathrm{Extrinsic}\mathrm{PEEP}+\mathrm{Intrinsic}\mathrm{PEEP}$$

Clinically, there is no single optimal PEEP value. The aim is to balance recruitment against overdistension while optimising oxygenation and carbon dioxide removal. The haemodynamic effects of transmitted positive pressure on the heart and great vessels must also be considered. Consequently, optimal PEEP is patient-specific.

Peak inspiratory pressure

Peak inspiratory pressure is the maximum airway pressure reached during inspiration. It is influenced by both resistive and elastic properties of the respiratory system and may change with inspiratory flow, flow profile, rise time, airway calibre, and tube obstruction.

Plateau pressure

Plateau pressure is measured during an end-inspiratory pause when flow has ceased. Under passive conditions it approximates alveolar pressure and reflects the pressure required to distend the respiratory system, rather than the resistive load of the airways.

Resistance

Resistance is the opposition to gas flow through the respiratory system, reflecting both the patient’s airways and the artificial circuit, including the endotracheal tube. Resistive pressure exists only during flow. For gas to move between the ventilator and the alveoli, these resistive forces must be overcome.

In passive conditions the total resistance of the respiratory system is estimated as:

$$\mathrm{Resistance}=\left(\begin{array}{l}\mathrm{Peak}\mathrm{inspiratory}\mathrm{pressure}-\\ \mathrm{Plateau}\mathrm{pressure}\end{array}\right)/\mathrm{Flow}$$

Increased resistance is seen in airway disease such as asthma, COPD, bronchospasm or in conditions that decrease the diameter of the airways such as secretions or tube obstruction.

During an end-inspiratory occlusion (when the inspiratory flow is zero), three pressures can be identified on the ventilator pressure waveforms:

• P0 (peak airway pressure): end-inspiratory pressure just before flow is zero, reflecting total pressure to overcome resistive and elastic forces.

• P1: pressure immediately after the rapid drop following occlusion. The fast decay from P0 to P1 represents dissipation of resistive pressure (airway resistance plus any pendelluft from gas redistribution between units with different time constants). P1 approximates elastic recoil but still contains a viscoelastic component.

• P2 (plateau pressure): pressure after full stabilisation during a prolonged occlusion (3–5 s). It represents true static elastic recoil.

Stress relaxation is the slow decline from P1 to P2, reflecting viscoelastic properties of the lung parenchyma and chest wall, whose tissues creep and redistribute stress at constant volume. It is time-dependent tissue behaviour, analogous to a stretched rubber band slowly losing tension at fixed length. P1 − P2 quantifies this viscoelastic component (sometimes called additional tissue resistance). In ARDS it can be appreciable, and partitioning the pressure across phases separates airway from tissue mechanics.

Resistances:

• (P0 − P1)/Flow: airway resistance (frictional component, plus any rapid pendelluft).

• (P0 − P2)/Flow: total respiratory system resistance (ohmic plus viscoelastic).

• (P1 − P2)/Flow: additional tissue resistance from stress relaxation.

In summary: P0 − P1 is the airway component, P1 − P2 the tissue component, and P0 − P2 the two combined (Figure 2).

Figure 2.

Partitioning of airway pressure into resistive and viscoelastic components during an end-inspiratory occlusion manoeuvre. Airway pressure is shown during controlled ventilation with a brief end-inspiratory pause (3–5 s). Peak airway pressure (P₀) reflects flow-dependent resistive and elastic components. On occlusion, pressure falls rapidly to P₁ as resistive pressure is abolished, followed by a slower decay to P₂ due to viscoelastic stress relaxation of the lung and chest wall. The pressure differences define mechanical components: (P₀ − P₁)/flow represents airway resistance (frictional component with any rapid pendelluft), (P₁ − P₂)/flow reflects additional tissue resistance from stress relaxation, and (P₀ − P₂)/flow represents total respiratory system resistance (ohmic plus viscoelastic). This partitioning separates airway and tissue contributions to respiratory mechanics and may be altered in acute respiratory distress syndrome.

Compliance and elastance

Elastance describes the tendency of the respiratory system to recoil. Compliance, its inverse, describes the ease with which it distends. A highly compliant system inflates easily (i.e. will gain more volume for the same unit of pressure), whereas a system with high elastance will require more pressure to be inflated with an additional unit of volume. Respiratory system compliance reflects the number of normally inflated alveolar units and physiologically a lung with more aerated alveolar units will have a greater compliance. Therefore, compliance is considered a proxy measure of functional residual capacity. However, when measured on the ventilator, the compliance of the respiratory system results from the combined behaviour of the lungs and chest wall.

The same airway pressure may have very different implications depending on the relative contribution of lung and chest wall mechanics.

Lung compliance is determined by the relationship between alveolar and intrapleural pressure (i.e., transpulmonary pressure), while chest wall compliance reflects the relationship between intrapleural and ambient pressure. Differentiating between these requires oesophageal manometry which allows estimation of transpulmonary pressure. This distinction is clinically important: the same airway pressure may be less injurious in patients with a stiff chest wall (e.g. obesity or abdominal hypertension), where pressure is preferentially transmitted to the chest wall, than in those with a compliant chest wall and poorly compliant lungs, in whom transpulmonary pressures may be excessive.

Dynamic compliance is measured during ongoing flow and is therefore influenced by both elastic and resistive forces. Static compliance is measured during zero flow, typically during an end-inspiratory hold, and better reflects the elastic properties of the respiratory system. In diseased lungs, however, even static measurements represent an average of multiple lung units with different regional mechanics.

$$\begin{array}{l}\mathrm{Static}\mathrm{compliance}=\mathrm{Tidal}\mathrm{volume}/\\ \left(\begin{array}{l}\mathrm{Plateau}\mathrm{pressure}-\\ \mathrm{total}\mathrm{End-expiratory}\mathrm{pressure}\end{array}\right)\end{array}$$

$$\begin{array}{l}\mathrm{Dynamic}\mathrm{compliance}=\mathrm{Tidal}\mathrm{volume}/\\ \left(\begin{array}{l}\mathrm{Peak}\mathrm{inspiratory}\mathrm{pressure}-\\ \mathrm{End-expiratory}\mathrm{pressure}\end{array}\right)\end{array}$$

Time constants

A time constant describes how quickly a lung unit fills or empties and is the product of compliance and resistance. Units with long time constants, as in obstructive disease, fill and empty slowly; units with short time constants, as in stiff injured lungs, do so rapidly. In practice, the lung contains many regions with different time constants, especially in ARDS and obstructive disease, which helps explain regional heterogeneity, gas trapping, and uneven ventilation.

Evidence for ventilation strategy

Targets and principles

The following is a selective overview of key studies underpinning current lung-protective ventilation practice rather than an exhaustive review of the literature. Many important trials, nuances, and areas of ongoing debate are beyond the scope of this article and will be explored in greater detail in subsequent articles. Lung-protective ventilation remains the central evidence-based approach to invasive ventilation in acute hypoxaemic respiratory failure. In ARDS, the ARDSNet ARMA trial showed improved survival with lower tidal volumes based on predicted body weight and with plateau pressure limited to 30 cmH2O or less. ⁸ Outside ARDS, lower tidal-volume strategies have also been associated with better clinical outcomes in many mechanically ventilated patients, although the effect size is smaller and patient selection is important.^9,10 Conservative oxygen strategies have not shown a clear mortality advantage over usual care in broad mechanically ventilated ICU populations, as shown in ICU-ROX and UK-ROX.^11,12 Similarly, higher PEEP strategies may improve oxygenation in selected patients with moderate-severe ARDS and possibly in those with recruitable lung, but trials such as ALVEOLI did not show a consistent mortality benefit when applied indiscriminately across all ARDS phenotypes. ¹³ Based on this data, recent ESICM guidelines did not recommend the routine use of higher PEEP in all patients with ARDS of all severities, ¹⁴ while the ATS guidelines recommend the use of higher PEEP only in moderate-severe ARDS. ¹⁵

The author’s interpretation of the current evidence is that protective ventilation should be viewed as a physiological framework rather than a single recipe. In practice, this involves using low tidal volumes, avoiding injurious pressures, minimising unnecessary hyperoxia, and individualising PEEP and mode selection according to respiratory mechanics, gas exchange, patient effort, and the clinical context.

Selecting ventilator mode

Ventilator Modes – overview

Ventilator modes can be described using three core characteristics. First, the control variable determines whether pressure or volume/flow is directly controlled. Second, the breath sequence describes whether breaths are spontaneous, assisted, intermittent mandatory ventilation or mandatory (controlled). Third, the targeting scheme describes how the ventilator achieves or adapts to its targets. This system can be used to describe all ventilator modes is known as the Taxonomic Attribute Grouping system and is particularly useful because manufacturer trade names are numerous and often obscure the underlying similarities between modes. ¹⁶

Control variable

Pressure control

In pressure-controlled ventilation (PCV), the clinician sets an inspiratory pressure, PEEP, respiratory rate, and inspiratory time. The ventilator therefore determines inspiratory pressure, while tidal volume and flow become dependent on respiratory mechanics (resistance and compliance) and, in assisted modes, patient effort. The resulting inspiratory flow is usually decelerating. Pressure control may improve synchrony and can be useful when limiting peak airway pressure is a priority, but it does not guarantee tidal volume. The decelerating flow pattern is thought to be more physiological than VC square wave and may improve gas distribution, pulmonary artery pressures, and oxygenation in poorly compliant lungs (Figure 3).^17,18

Figure 3.

Pressure- and volume-controlled ventilation waveforms, representative flow-time, pressure-time, and volume-time curves for pressure-controlled ventilation (PCV) and volume-controlled ventilation (VCV). In PCV, a square-wave pressure profile produces decelerating inspiratory flow and a negatively exponential volume-time curve. In VCV, fixed tidal volume is delivered using either constant (square-wave) or decelerating (reverse-ramp) flow, generating rising or negatively exponential pressure-time curves, respectively.

It is worth noting, that in both pressure and volume control the ventilator is delivering flow. In pressure control it is simply adjusting flow on a millisecond-by-millisecond basis to target an exact pressure.

Volume control

In volume-controlled ventilation, the clinician sets tidal volume and typically inspiratory flow or inspiratory time. Delivered tidal volume is therefore guaranteed, whereas airway pressure depends on respiratory mechanics and may rise substantially if compliance worsens or resistance increases. Classical volume control uses a square-wave inspiratory flow, although modern ventilators may also provide decelerating flow profiles. The downside to this is the potential for higher strain and less homogeneous flow in patients with significantly diseased lungs. Volume control is often preferred when tight control of minute ventilation or tidal volume is required, but pressure must be monitored carefully.

Breath sequence

Spontaneous

In spontaneous modes, both triggering and cycling are determined by the patient. The ventilator may provide little more than PEEP or CPAP, or may add compensation for the resistive load of the artificial airway, for example with automatic tube compensation in selected ventilators (Figure 4). ¹⁹

Figure 4.

Breath sequencing: spontaneous, intermittent mandatory ventilation and mandatory ventilation. Representative breath sequences across ventilatory modes. In spontaneous modes, patient inspiratory effort generates a negative pressure or flow, resulting in unassisted breathing or triggering pressure- or volume-assisted support. In synchronised intermittent mandatory ventilation (SIMV), the ventilator guarantees a minimum minute ventilation through a combination of patient-triggered assisted breaths and time-cycled mandatory breaths. In mandatory (controlled) ventilation, all breaths are time-cycled and delivered by the ventilator independent of patient effort.

Assisted

In assisted modes, the ventilator augments a patient-triggered breath. The commonest ICU example is pressure-support ventilation, in which a preset pressure above PEEP is delivered during inspiration. Assisted ventilation can reduce the work of breathing while preserving respiratory muscle activity and is therefore central to weaning. More advanced forms of assistance include NAVA, which uses the diaphragm electrical activity as the control signal, ²⁰ and proportional assist ventilation (PAV), in which ventilator output increases in proportion to estimated patient effort. ²¹

Intermittent mandatory ventilation (IMV)

Intermittent mandatory ventilation (IMV) is a breath sequence in which a predefined number of mandatory breaths are delivered while allowing spontaneous breaths to occur between them, independent of the underlying control variable. In modern synchronised IMV (SIMV), mandatory breaths are delivered within a defined inspiratory trigger window, during which patient effort can synchronise the mandatory breath, while spontaneous breaths may occur outside this window and are often supported with pressure support; an expiratory window permits spontaneous breathing without triggering a mandatory breath. In contrast, non-synchronised IMV delivers mandatory breaths irrespective of patient effort or timing windows, predisposing to breath stacking, increased work of breathing, and significant patient–ventilator dyssynchrony, and is therefore largely obsolete in contemporary practice.

Mandatory ventilation

In mandatory ventilation, breaths are delivered irrespective of whether the patient is making inspiratory efforts. In practice this often requires substantial sedation and, in some situations, neuromuscular blockade. Controlled ventilation may be useful early in severe respiratory failure, in profound dyssynchrony, or when strict control of PaCO2 and cerebral vasculature is needed.

Neuromuscular blockade should not be viewed as a routine adjunct to ventilation. Although the ACURASYS trial suggested benefit in early severe ARDS, ²² the larger ROSE trial did not confirm an improvement in mortality or ventilator-free days with a strategy of routine early continuous neuromuscular blockade. ²³ Deep sedation is also associated with adverse outcomes, and prolonged paralysis contributes to ICU-acquired weakness. ²⁴

Targeting scheme

Set point

The clinician sets the ventilatory targets directly and the ventilator delivers them without automatic adaptation. E.g. deliver 500 ml on volume-control ventilation. This remains the simplest and most transparent targeting scheme (Figure 5).

Figure 5.

Ventilator targeting schemes. Summary of ventilator control strategies. Set-point (s) modes deliver clinician-defined settings without adaptation. Dual control (d) permits within-breath switching between pressure and volume targets. Servo (r) control provides assistance proportional to patient effort (e.g. PAV+). Adaptive (a) modes adjust targets between breaths in response to changing mechanics (e.g. PRVC, Autoflow). Bio-variable (b) modes introduce breath-to-breath variability. Optimal (o) targeting uses algorithms to optimise a performance function (e.g. ASV). Intelligent (i) targeting incorporates artificial intelligence to continuously adjust support (e.g. SmartCare™, INTELLiVENT-ASV®).

Dual control. Dual control combines pressure- and volume-targeted ventilation within a single mode. The ventilator can switch between control strategies to achieve a predefined target. For example, in volume-assured pressure support (VAPS), inspiration begins as a pressure-supported breath. If the target tidal volume is not achieved, the ventilator continues inspiration using volume-targeted delivery until the preset volume is reached.

Servo

In servo targeting, ventilator output follows a varying input signal, so that assistance is proportional to patient activity or demand. PAV and NAVA are examples of servo-controlled support.

Adaptive

In adaptive targeting, the ventilator modifies one or more settings between breaths in response to measured changes in mechanics or ventilation. Examples include pressure-regulated volume control (PRVC) in which compliance is calculated on the previous breath, and the subsequent breath is delivered at a different pressure to achieve a set tidal volume.

Bio-variable

Bio-variable modes deliberately introduce variability into tidal volume, pressure, or timing to mimic some of the breath-to-breath variability seen during normal spontaneous breathing. Note this is primarily academic and rarely used in clinical practice.

Optimal

(In optimal targeting, the ventilator uses an algorithm to select a breathing pattern that achieves a predefined goal. This may include minimising the work of breathing or the pressure required to achieve a target minute ventilation (e.g. Hamilton’s ASV utilising the Otis’ equation).

Intelligent

Targeting scheme that uses rule-based automation or artificial intelligence-derived logic to adjust support according to changing physiological inputs and predefined clinical goals, as in systems such as SmartCare/PS or IntelliVent-ASV.

Advanced modes of ventilation

Although all modes can be described within the taxonomy above, some advanced modes merit specific explanation because they are often encountered in ICU practice and are frequently misunderstood.

Airway pressure release ventilation (APRV)

Airway Pressure Release Ventilation (APRV) is a pressure-controlled mode designed to improve oxygenation while limiting ventilator-induced lung injury through sustained alveolar recruitment. It applies a prolonged high airway pressure (PHigh) to stabilise alveoli and increase mean airway pressure, interrupted by brief pressure releases that facilitate carbon dioxide clearance. By minimising cyclic alveolar collapse and overdistension, APRV aims to reduce atelectrauma and improve the homogeneity of lung inflation. ²⁵

A key physiological advantage of APRV is the allowance of spontaneous breathing throughout the ventilatory cycle, which may improve ventilation–perfusion matching, preserve diaphragmatic function, and reduce the need for deep sedation or neuromuscular blockade. The release phase (Tlow) is typically short and individualised according to respiratory mechanics, often being terminated when expiratory flow decays to approximately 75% of peak expiratory flow. This approach limits lung emptying, generates intrinsic PEEP, and reduces derecruitment while maintaining effective ventilation. As lung compliance improves during recovery and respiratory time constants lengthen, Tlow should be progressively adjusted to accommodate longer release phases. Drager (AutoRelease) function automatically sets Tlow to 0.75% peak expiratory flow, thus limiting clinician input.

Clinical and physiological data suggest that APRV can improve oxygenation and increase ventilator-free days compared with conventional lung-protective ventilation in patients with ARDS, although a consistent mortality benefit has not been demonstrated. ²⁶

Advanced closed loop

Closed-loop ventilation modes automatically adjust breath parameters in response to real-time measurements of respiratory mechanics to achieve a target minute ventilation while minimising patient work of breathing. The clinician sets the therapeutic goal (e.g. predicted minute ventilation) and safety limits for pressure and tidal volume, and the ventilator calculates an optimal breathing frequency and dynamically modulates tidal volume, pressure support, and respiratory rate to meet the target.

Examples include Adaptive Support Ventilation (ASV, Hamilton Medical), which adjusts ventilation based on compliance and resistance, IntelliVent-ASV, which additionally automates oxygen and PEEP titration, and SmartCare/PS (Dräger), which guides pressure support during weaning. These modes are particularly useful for weaning patients from mechanical ventilation, as they can reduce patient effort and maintain stable ventilation.

Clinical trials of closed-loop modes such as Adaptive Support Ventilation (ASV) have demonstrated reductions in weaning time compared with conventional pressure support ventilation in selected populations. ²⁷ Systematic reviews indicate that automated weaning systems, including SmartCare/PS, may reduce the duration of weaning and overall ventilation compared with non-automated strategies, but evidence is heterogeneous and of mixed quality. ²⁸ In direct comparisons with clinician- or physiotherapist-driven weaning protocols, SmartCare/PS did not consistently reduce weaning or ventilation duration, and no automated system has proven superior to skilled, protocolised weaning supervised by experienced clinicians.^29,30

Summary

This article has reviewed the ventilator breath cycle, core physiological concepts, and a practical framework for understanding ventilator modes independent of manufacturer-specific terminology. Safe mechanical ventilation requires an understanding of pressure, flow, volume, timing, and patient–ventilator interaction, together with an appreciation of how respiratory mechanics influence ventilator behaviour. These principles provide the foundation for selecting and interpreting ventilator settings at the bedside.

The next article in this series will examine the evidence underpinning contemporary ventilatory strategies in the ICU, with a particular focus on the avoidance of injurious ventilation, the mechanisms of ventilator-induced lung injury, and the application of lung-protective ventilation in patients with acute respiratory distress syndrome (ARDS). An understanding of ventilator mechanics is essential for the application of evidence-based lung-protective ventilation.