Learning objectives

After reading this article, you should be able to:

C describe the features of a ventilatory mode which distinguish it

from other modes

C list the indications and complications of invasive and non

invasive ventilation

INTENSIVE CARE

Ventilatory support in theintensive care unitMartin Hughes

Jane Kyle

Abigail Short

C describe the most commonly used adjuncts to mechanical

ventilation

AbstractThis article focuses on a classification of modes of mechanical ventilation,

the indications for and complications of invasive and non-invasive me-

chanical ventilation and the recent evidence on adjuncts to mechanical

ventilation.

Keywords Adjuncts to mechanical ventilation; non-invasive ventilation;

positive pressure respiration; ventilators mechanical (classification)

Royal College of Anaesthetists CPD matrix: 2A05, 2C02, 2C04, 2C05, 3C00

Classification of ventilators

Positive pressure ventilators

Ventilator modes may be classified according to mode of trig-

gering, inspiratory characteristics, mode of cycling, the pattern

of mandatory and spontaneous breaths and method of

synchronization.

Expiration is passive in all modes except high-frequency

oscillation. Positive end expiratory pressure (PEEP) is almost

always applied in critically unwell patients. It increases func-

tional residual capacity, recruits alveoli, reduces shunt, helps

prevent atelectrauma and reduces preload and afterload. A full

discussion of the best way to set the level of PEEP is outwith the

scope of this article.

Mode of triggering: triggering is the start of inspiration. Venti-

lators measure pressure, volume, flow and time. Inspiration is

triggered when one of these variables reaches a preset value.

Breaths may be triggered by the patient or ventilator. If the res-

piratory rate is set at 10/minute, a controlled mechanical breath

will be commenced every 6 seconds (time triggering). For

patient-triggered breaths, it is usually a change in flow or

Martin Hughes MB ChB BSc MRCP FRCA Consultant in Anaesthesia and

Intensive Care, Royal Infirmary, Glasgow, UK. Conflicts of interest:

none.

Jane Kyle MB ChB MRCP LAT 2 Anaesthesia, Royal Infirmary, Glasgow, UK.

Conflicts of interest: none.

Abigail Short MB ChB BSc (Hons) MRCP CT2 Anaesthesia Royal Infirmary,

Glasgow, UK. Conflicts of interest: none.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:10 466

pressure which results in the start of a supported spontaneous

breath (e.g. pressure support ventilation (PSV)) or a mandatory

breath (e.g. synchronized intermittent mandatory ventilation

(SIMV) in the synchronization window (see below), or assist

control ventilation (ACV)). Alternate triggers are possible (e.g.

diaphragmatic contraction or chest wall motion in children).

Inspiratory characteristics:

Control mode e ventilators are either pressure controllers, or

flow (or volume) controllers. In practice flow and volume con-

trollers behave almost identically (direct control of flow means

indirect control of volume and vice versa) and both are called

‘volume-controlled ventilation’ (VCV). Most VCV uses flow

control.

Figure 1 demonstrates the difference between a pressure-

controlled and a volume-controlled breath.

With pressure control, inspiratory pressure is chosen by the

clinician (2b). Flow in a passive patient is decelerating (2a). With

increasing patient effort sine wave flow becomes more promi-

nent. Airway pressure is controlled, but the volume delivered

depends on respiratory system impedance and inspiratory time

(2c).

Usually with volume control, TV and inspiratory flow are

chosen by the clinician (1a) (inspiratory flow is often set indi-

rectly by choosing the respiratory rate, inspiratory:expiratory

(I:E) ratio and tidal volume e.g. RR 20, I:E 1:2, TV 600 ml ¼ 3

seconds per breath, 1 second for inspiration, therefore inspira-

tory flow of 36l/minute; 1a). Delivered volume is controlled, but

airway pressure is dependent on compliance and resistance (for

peak pressure, A) and compliance (for plateau pressure, B) (1b).

No benefit in significant outcomes has ever been demon-

strated for either mode over the other, and many of the trials of

mechanical ventilation use volume-controlled modes. Compared

with VCV, PCV has the following theoretical advantages:

� Alveolar pressure is limited and cannot be higher than the

set inspiratory pressure.

� Peak airway pressures will be lower for an equivalent tidal

volume.

� For a given peak airway pressure, mean airway pressure is

higher. Oxygenation may therefore be improved (but will

also depend on the plateau pressure and PEEP).

� There may be improved distribution of ventilation. There

is less end inspiratory gradient of pressure among regional

units with heterogeneous time constants. CO2 elimination

is improved.

� 2013 Elsevier Ltd. All rights reserved.

Flow

1a

x

ti te

2a

x

ti te

Circuitpressure

1b

x

A

B

ti te

2b

x

ti te

Alveolarvolume

1c

x

ti te

2c

x

ti te

x = no flow; A = peak pressure; B = plateau pressure; ti = Inspiratory time; te = expiratory time.

Figure 1 Pressure-controlled ventilation (2aec) versus volume-controlled ventilation (1aec).

INTENSIVE CARE

The main disadvantage of PCV is the variation in tidal vol-

ume. In addition, when there is vigorous patient inspiratory

effort, pleural pressure drops significantly and the trans-

pulmonary pressure (the pressure responsible for alveolar strain

and ventilator-induced lung injury, (VILI)) may be high.

Studies demonstrate that the incidence of ventilator-induced

lung injury is unchanged and there are similar haemodynamic

consequences.

Modern ventilators can deliver breaths with characteristics of

both types of breath, called dual control or hybrid breaths (e.g.

pressure-regulated volume control, where pressure control and

ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:10 467

decelerating flow patterns are combined with volume cycling).

These modes have the theoretical advantages of pressure

controlled breaths, but with more accurate volume control. It is

also possible to alter the flow characteristics of volume control

breaths on some ventilators e various profiles have been

described, for example decelerating or sinusoidal. Definitive ad-

vantages of specific flowetime profiles (lower peak pressures or

more homogeneous gas distribution) are not clearly established.

Limit: the term limit refers to any variable which reaches a preset

value before inspiration ends. It sustains inspiration. ‘Limit’ is

� 2013 Elsevier Ltd. All rights reserved.

Indications for invasive ventilation

C HypoxaemiaC Hypoxaemia in the absence of hypercapnia or exhaustion may

be due to unilateral shunt. Positive pressure ventilation in

unilateral lung disease may paradoxically worsen shunt by

forcing blood from compliant areas to consolidated areas

C Hypercapnia

C PaCO2 above 10 kPa (75 mmHg) is unlikely to be adequately

treated with non-invasive ventilation. Hypercapnia causing

neurological impairment should be treated with invasive

ventilation

C ExhaustionC This is the commonest indication for ventilation

C To reduce oxygen consumption

C If there is evidence of oxygen supply demand imbalance

(acidosis, high lactate, low ScVO2) and high respiratory work

C To protect the airway

C To treat or prevent an obstructed airway

C To facilitate investigations, e.g. CT

C To facilitate treatment of other conditions, e.g. GI bleeding

C For transfer

Table 1

INTENSIVE CARE

sometimes interchangeable with ‘control’, for example pressure-

controlled breaths are equivalent to pressure-limited breaths

which are equivalent to pressure-targeted breaths. This termi-

nology may also lead to confusion: the phrase ‘volume limited’

usually means flow limited and volume cycled (VCV).

Mode of cycling: cycling is the method the ventilator uses to end

inspiration and allow expiration to start. Expiration is passive.

Cycling is also called expiratory triggering and occurs when a

preset value of flow, time, volume (or pressure) is reached.

Mandatory breaths are generally time cycled (PCV) or volume

cycled (VCV). Spontaneous supported breaths (PSV) are usually

flow cycled (expiration usually starts at 25e33% of peak inspi-

ratory flow. This is adjustable on many ventilators).

Pressure cycling is now only used as a safety backup for other

forms of cycling, that is, it will terminate the breath if pressure

rises to a preset level.

Pattern of mandatory and spontaneous breaths, and patient

ventilator synchrony: mandatory breaths are machine triggered

and/or cycled. Mandatory breaths that are patient triggered are

called assisted.

Spontaneous breaths are patient triggered and cycled. Spon-

taneous breaths may be supported or unsupported.

Synchrony is the agreement between the patient’s own

(neural) and the ventilator (mechanical) inspiratory and expira-

tory time, and includes the matching of patient effort with

delivered tidal volume (more effort should result in increased

volume). Each mode of ventilation has specific rules governing

interaction with the patient. These rules are made clear in all

ventilator manuals, and a full discussion of this subject is out-

with the scope of this article. As an example we will examine the

differences between P-SIMV and bi-phasic positive airway pres-

sure (BIPAP).

P-SIMV and BIPAP are identical in a passive patient.

In an active patient, patient ventilator interaction during expi-

ration is the same. There are two expiratory timewindows. During

the first period of expiration, the patient is allowed to breathe

spontaneously or with support (PSV). During the second (syn-

chronization) window, patient effort will trigger a time-cycled

mandatory breath. In essence, the mandatory breath which was

due is delivered early to coincide with patient inspiratory effort.

The modes, however, differ markedly during inspiration.

With BIPAP, the patient can breathe throughout inspiration (with

a floating valve opening to prevent excessive airway pressure).

Patient efforts are allowed, and superimposed on the time-cycled

inspiratory pressure. Cycling to expiration is also synchronized

with patient expiration. With P-SIMV, patient effort is unrecog-

nized during inspiration, and may result in breath termination

due to a breach of the high-pressure safety limit.

Method of synchronization: it is important to recognize that no

current mode of ventilation that uses pneumatic signals to trigger

and cycle (including modes such as PSV/ASB) is without sig-

nificant synchrony problems. Difficulties include inspiratory

trigger delay, ineffective triggering, double triggering, auto trig-

gering, inspiratory time extension, early expiratory cycling and

failure of expiratory cycling. Neurally adjusted ventilatory assist

(NAVA) may reduce some of the common difficulties by using

ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:10 468

diaphragmatic contraction to trigger breaths and to guide support

levels. Proportional assist ventilation is claimed to decrease the

likelihood of triggering delay, ineffective efforts and expiratory

asynchrony, while promoting sleep efficiency and breathing

stability.

Invasive ventilation

Invasive ventilation should be considered when non-invasive

ventilation has failed or has been deemed inappropriate. The

commonest indications and potential complications of invasive

ventilation are described in Tables 1 and 2.

Ventilator-induced lung injury

Ventilation is often a life-saving procedure, but there are signif-

icant complications. The most common and probably most

important of these is ventilator-induced lung injury (VILI). This

term encompasses barotrauma (injury due to excessive pressure)

and volutrauma (injury due to excessive volume) e in combi-

nation these produce alveolar strain (defined as the ratio be-

tween the amount of gas volume delivered compared with the

amount of aerated lung receiving it). Crucially, damage is also

caused by atelectrauma (injury due to repeated opening and

closing of alveoli) and biotrauma (distal organ dysfunction

caused by release of inflammatory mediators because of VILI).

Preventing VILI is difficult and the best way to do so is not

established. In acute respiratory distress syndrome (ARDS),

avoid plateau pressures over 30 cmH2O, use tidal volumes of no

more than 6 ml/kg of ideal body weight, select PEEP to prevent

end expiratory alveolar closure without increasing alveolar strain

(see further reading), and perhaps use intermittent recruitment

manoeuvres. These techniques, in combination with permissive

hypercapnia and permissive hypoxia, are together termed ‘lung

protective ventilation’.

� 2013 Elsevier Ltd. All rights reserved.

Complications of invasive ventilation

Complications of endotracheal tubeC Ventilator-associated pneumonia

C Tracheal stenosis

C Vocal cord injury

C Tracheo-oesophageal fistula

C Sinusitis

Complications of mechanical ventilation

C Ventilator-induced lung injury

C Air leaks including bronchopleural fistulae

C O2 toxicity

C Reduction in cardiac output

C Reduction in renal or splanchnic blood supply

C Fluid retention (increased renin, angiotensin, aldosterone and

antidiuretic hormone, reduced ANP)

C Ventilator-induced diaphragmatic dysfunction

Complications due to immobility

C Venous thromboembolism

C Pressure sores

Complications related to critical illness

C GI bleeding

C GI dysmotility

C Endocrine disease

C Polymyoneuropathy

Table 2

INTENSIVE CARE

In concept, high-frequency oscillatory ventilation seemed the

ideal way to achieve these ends, but two recent trials have sug-

gested that at best, outcomes are not improved, or that mortality

may be worse when using this technique on unselected patients

with ARDS.1,2

Non-invasive ventilation

The term non-invasive ventilation (NIV) includes continuous

positive airway pressure (CPAP) and bi-phasic positive airway

pressure (BIPAP). Both can be delivered via a facemask, nasal

mask or hood.

CPAP

Indications for non-invasive ventilation

C Acidotic, hypercapnic exacerbation of chronic obstructive pul-

monary disease (COPD)

C Elective non-invasive ventilation post-extubation in patients

with COPD, patients who are hypercapnic pre-extubation, or

patients who are likely to require long-term ventilation

C Cardiogenic pulmonary oedema (CPAP)

C Thoracic wall deformities, e.g. kyphoscoliosis

C Obesity hypoventilation syndrome

C Acute neurological disease (e.g. GuillaineBarre syndrome,

CPAP delivers positive pressure throughout spontaneous venti-

lation where there is no additional pressure augmentation during

inspiration. In responsive diseases (e.g. cardiogenic pulmonary

oedema where oxygenation, and not CO2 clearance, is usually

more problematic) it recruits alveoli, increases the functional

residual capacity, reduces shunt, increases V/Q ratio and im-

proves oxygenation. It may reduce work of breathing by moving

the lungs to a steeper (more compliant) position on the pressure

volume curve. At high levels it can cause overdistension, in-

crease pulmonary vascular resistance, and reduce right and left

ventricular output.

although invasive ventilation is usually required)

C Progressive neurological disease (e.g. motor neurone disease)

BIPAP C Status asthmaticus (little evidence)

C Patients ’not for intubation’, but who require respiratory support

Table 3

The nomenclature surrounding BIPAP can be confusing. Com-

mercial trademarking means that BIPAP is also termed Bi-Vent

(Servo i), BIPAP (Drager Evita XL), BiLevel (Puritan Bennett),

BiPhasic (Viasys Avea), and DuoPAP (Hamilton). It is not to be

ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:10 469

confused with bilevel positive airway pressure (BiPAP), a non

invasive ventilation system offered by Respironics (Carlsbad, CA).

In BIPAP, patient efforts are augmented by an inspiratory

positive airways pressure (IPAP). By convention, the expiratory

positive airways pressure is called EPAP rather than PEEP.

Breaths are normally flow triggered, pressure limited and flow

cycled. Time triggering and cycling may be used if controlled NIV

is necessary (usually for neuromuscular diseases).

The indications and potential complications for NIV are listed

below in Tables 3 and 4. Its success depends upon appropriate

patient selection, early intervention and recognizing when it

no longer provides adequate support. As well the effects of

increased intrathoracic pressure (CPAP, above), the additional

positive inspiratory pressure reduces work of breathing, im-

proves tidal volumes, reduces respiratory rate, and increases CO2

clearance. It is therefore more effective than CPAP in treating

type 2 respiratory failure e.g. an acute exacerbation of COPD.

Contraindications to NIV include agitated or uncooperative

patients, those patients with an inability to protect their own

airway, facial/oesophageal/gastric surgery, craniofacial trauma

or thick copious secretions.

The patient ventilator interface is usually amask, but hoods are

available as an alternative. Some patients prefer them, but trig-

gering and cycling problems are common. Increasing the delivered

pressures (both PEEP/EPAP and inspiratory pressure/IPAP) re-

duces, but does not eliminate, these problems. (Tables 3 and 4)

Adjunctive therapies

Extracorporeal membrane oxygenation (ECMO)

ECMO is a system where O2 is added to and CO2 removed from

the blood in a gas exchange membrane separate from the lungs.

It can be veno-venous (the usual route for respiratory support),

or arterio-venous, depending on the design of the circuit and

where the large cannulae are placed. It is highly specialized and

very labour intensive. ECMO allows the lungs to be ‘rested’ with

low volume and pressure ventilatory support.

The results of the CESAR trial3 suggest that referral of adults

with refractory hypoxaemia to a tertiary centre which can pro-

vide specialist support, including ECMO, will increase disability

free survival at 6 months (63% versus 47%, relative risk 0.69,

� 2013 Elsevier Ltd. All rights reserved.

Complications of non-invasive ventilation

C Failure to improve hypoxaemia

C Gastric insufflation

C Aspiration

C Delayed intubation

C Patient discomfort

C Facial pressure sores and necrosis

Table 4

INTENSIVE CARE

95% confidence intervals 0.05e0.97). About 25% of the patients

transferred did not receive ECMO, and there was no standardi-

zation of treatment in the control group. It is possible that the

beneficial effect was produced by treatment in a regional centre,

rather than ECMO itself. Referral to an ECMO centre should be

considered at an early stage when lung protective ventilation

with adjunctive therapies cannot provide acceptable gas

exchange.

Prone position

The physiological rational behind prone positioning is to improve

homogenous distribution of aeration within the ventilated lung.

Pressure from mediastinal and abdominal compartments is alle-

viated thereby reducing the volume of non-aerated regions in the

well-perfused dorsal lung.4 The compliance of both newly

recruited regions of lung and non-diseased lung is more equal

and ventral hyperinflation is limited thus reducing propensity to

ventilator-induced lung injury (VILI). These improvements are

more pronounced in lobar ARDS.

As a rescue technique, it has been shown to improve

oxygenation in patients with ARDS. A recent study has demon-

strated a reduction in both 28 and 90-day mortality in patients

with severe ARDS.5 Proning was initiated early and continued for

18 hours a day (for an average of 4 days). This is compatible with

previous meta-analyses suggesting an improved outcome in se-

vere ARDS.

The quoted complication rate of prone positioning varies. This

is a technical skill and the coordination of the team will have an

impact. Risks include pressure sores in new weight-bearing

areas, displacement or obstruction of endotracheal tubes,

drains or catheters and facial and periorbital oedema.

Intensive care unit teams should develop the expertise to

provide safe care in the prone position for those patients with

severe ARDS who cannot be safely or effectively ventilated using

lung protective ventilation.

Paralysis

Recent research has suggested that early use of the benzoqui-

nolonium neuromuscular blocker cisatracurium for a 48-hour

time period was associated with an improved 90-day survival

in a population adjusted for severity of hypoxaemia (PaO2:FiO2

<120). This population also demonstrated increased ventilator

free time and a reduced risk of barotrauma. There was no sig-

nificant increase in muscle weakness.6

This was surprising, and if the results are robust and repeat-

able, would herald a significant change in ventilator strategy for

many e away from the maintenance of spontaneous breathing in

various forms for ARDS.

ANAESTHESIA AND INTENSIVE CARE MEDICINE 14:10 470

There are several potential mechanisms by which neuro-

muscular blockade might improve survival. It is unlikely to be

related to improved gas exchange (since gas exchange in the two

groups was similar). It is more likely to be as a result of a

reduction on VILI as a result of improved control of inspiratory

and expiratory pressures and volumes, and decreased patient

ventilator asynchrony.

Currently, it would be reasonable to add neuromuscular

blockade to patients with severe ARDS, who have any degree of

patient ventilator asynchrony, or who are in the prone position.

Fluid therapy

Fluid restriction (aiming for central venous pressure< 4 cmH2O,

achieving an even fluid balance with or without diuretics and using

vasoconstrictors for blood pressure maintenance) in ARDS

following the initial phase of 48 hours of resuscitation has been

shown to reduce length of ventilation without increasing other

organ damage. Mortality is unchanged.7 Most experts would

recommend aggressive diuresis/fluid removal, even at the expense

of other organ perfusion, in the face of refractory hypoxaemia.

Nitric oxide

Nitric oxide (NO) improves ventilation-perfusion mismatch by

causing pulmonary vasodilation in capillaries supplying venti-

lated alveoli.

The Cochrane Collaboration in 2013 concluded that NO was

effective in transiently improving oxygenation in the first 24

hours with no statistically significant effect on mortality in all

ages of patient with acute hypoxaemic respiratory failure.8 It also

comments on an increased risk of renal failure. When used for

ARDS, there is no traditional dose response curve. Low doses

may be safer and potentially more effective at improving

oxygenation than higher doses.9

NO is an effective treatment for pulmonary artery

hypertension.

It may reasonably be used as a rescue therapy for patients

dying of refractory hypoxaemia.

There has been no outcome benefit demonstrated for partial

liquid ventilation, rotational therapy, tracheal gas insufflation,

treatment for pulmonary artery hypertension (such as sildenafil

or prostacyclin), b agonists, surfactant, or Heliox.

Severe ARDS

Patients with severe ARDS should be managed differently from

the larger group with moderate or mild ARDS. Lung protective

ventilator strategies should be used (as with all ARDS patients),

but in addition prone position and paralysis should be employed

at an early stage in those patients who do not respond to more

simple interventions. Aggressive fluid restriction should be

instituted as early as possible. If these measures fail, refer to a

regional ECMO centre. A

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� 2013 Elsevier Ltd. All rights reserved.

INTENSIVE CARE

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FURTHER READING

Chatburn RL. Classification of mechanical ventilators. In: Tobin MJ, ed.

Principles and practice of mechanical ventilation 2006; 37e52.

Hughes M, Black RG, eds. Advanced respiratory critical care. Oxford Uni-

versity Press, 2011. http://ukcatalogue.oup.com/product/

9780199569281.do.

Pinsky MR. Heart lung interactions. Curr Opin Crit Care 2007; 13: 528e31.

� 2013 Elsevier Ltd. All rights reserved.