Basic concepts in mechanical ventilation.
Abstract: Mechanical ventilatory support is a major component of the clinical management of critically ill patients admitted into intensive care. Closely linked with the developments within critical care medicine, the use of ventilatory support has been increasing since the polio epidemics in the 1950s (Lassen 1953). Initially used to provide controlled mandatory ventilation, today with advances in technology, most mechanical ventilators are triggered by the patient, increasing the awareness of the complexity of patient/ventilator interaction (Tobin 1994). Though ventilator appearance and design may have changed quite significantly and the variety of options for support extensive, the basic concepts of mechanical ventilatory support of the critically ill patient remains unchanged. This paper aims to outline these concepts so as to gain a better understanding of mechanical ventilatory support.

KEYWORDS Oxygenation / Respiration / Ventilation

Key points

1. Mechanical ventilation is indicated when less invasive treatment methods for hypoxic or hypercapnic respiratory failure are unsuccessful.

2. The primary goals of mechanical ventilation are support of the ventilatory and oxygenation functions of the lung and reducing work of breathing, while assuring patient comfort.

3. Various types of breaths and modes of ventilation are available to facilitate synchrony between the patient and ventilator.

4. Important monitoring during mechanical ventilation includes attentive physical assessment of the patient, respiratory function (patient/ventilator synchronisation, chest auscultation, airway (patency, secretions, pressures), breathing (rate, volume, oxygenation), arterial blood gas (ABG) measurements chest radiography (CXR)).
Subject: Acute respiratory distress syndrome (Care and treatment)
Acute respiratory distress syndrome (Research)
Artificial respiration (Methods)
Artificial respiration (Health aspects)
Author: Carbery, Catherine
Pub Date: 03/01/2008
Publication: Name: Journal of Perioperative Practice Publisher: Association for Perioperative Practice Audience: Academic Format: Magazine/Journal Subject: Health; Health care industry Copyright: COPYRIGHT 2008 Association for Perioperative Practice ISSN: 1750-4589
Issue: Date: March, 2008 Source Volume: 18 Source Issue: 3
Topic: Event Code: 310 Science & research
Geographic: Geographic Scope: Australia Geographic Code: 8AUST Australia
Accession Number: 193344196
Full Text: Indications for initiation of mechanical ventilatory support

The primary indications for the initiation of mechanical ventilatory support are acute respiratory failure (including acute respiratory distress syndrome, heart failure, sepsis, pneumonia, complications of surgery and trauma), coma, acute exacerbation of chronic obstructive pulmonary disease (COPD) and neuromuscular disorders. (Esteban et al 2000) The primary objectives of mechanical ventilation are improvement of alveolar ventilation, decreasing the work of breathing and reversing life threatening hypoxemia or acute respiratory acidosis (Tobin 2001). Table 1 outlines physiological and clinical objectives.

The clinician must consider history, physical assessment, arterial blood gas analysis, appropriate lung mechanics and patient prognosis when deciding whether to intubate and mechanically ventilate. This decision must be based on evidence that the intervention will be beneficial and associated with good patient outcome, for example, improved quality of life or a lower mortality rate.

Acute respiratory failure

Probably the most common reason for instituting mechanical ventilation is decreasing the inspiratory effort and risk of inspiratory-muscle fatigue, which is significantly increased in patients with acute respiratory failure.

If a person cannot maintain normal ventilation and has inadequate exchange gases, cardiopulmonary arrest may be imminent and intervention is required immediately. In acute respiratory failure, respiratory effort is absent or insufficient ensure adequate uptake of oxygen or clearance of carbon dioxide. Clinically, acute respiratory failure may be defined as:

(a) Pa[O.sub.2] less than predicted normal range for patient's age or 60mmHg (8kPa)

(b) PaC[O.sub.2] greater than 50mmHg (7kPa) and rising

(c) falling pH 7.25 and lower

Respiratory failure is divided into two forms:

* Type 1 respiratory failure is defined as hypoxia without hypercapnia (C[O.sub.2] level may be normal or low). It is typically caused by a ventilation/perfusion (V/Q)mismatch, but may also occur with right-left shunting, alveolar hypoventilation, aging and inadequate inspired oxygen.

* Type 2 respiratory failure is defined as a build up of carbon dioxide that has been generated by the body.

Three types of disorders can lead to acute hypercapnic respiratory failure:

* CNS disorders

* Neuromuscular disorders

* Disorders that increase work of breathing (WOB)

Table 2 outlines the indications for mechanical ventilation in acute respiratory failure.

Mode of ventilation and breath delivery

The pattern of breath delivery and breath type during mechanical ventilation constitutes the mode of ventilation. Factors determining the mode are:

* Type of breath--mandatory, spontaneous, assisted.

* Target control variable--volume, pressure.

* Timing of breath delivery--Continuous mandatory ventilation (CMV). Synchronised intermittent mandatory ventilation (SIMV) or Spontaneous.

Types of ventilator breaths

Ventilator breaths can be simply classified as mandatory, spontaneous or assisted. Spontaneous breaths are both initiated and terminated by the patient. The patient, dependent on demand and lung characteristics, controls timing and tidal volume. When the ventilator controls the tidal volume delivery and timing, the breath is considered mandatory. Assisted breaths have characteristics of both spontaneous and mandatory breaths. Patient initiated breaths are assisted to reach a preset target pressure.

The most commonly used types of ventilator breaths are best differentiated by the cycling mechanism. The cycle variable is usually the volume, time or flow that terminates inspiration (closure of inspiratory valve and opening of expiratory valve). When the set peak pressure limit is exceeded, pressure may be the cycling variable that terminates inspiration.

Volume-cycled breath (volume breath)

The type of breath assures the delivery of a present tidal volume (unless the peak pressure limit is exceeded). With most ventilators, the setting of peak inspiratory flow rate and choice of inspiratory flow waveform (square, sine or decelerating) determine the length of inspiration. Some ventilators adjust inspiratory flow as lung resistance and compliance change to maintain not only the preset tidal volume but also a present inspiratory time. With volume-cycled breaths, worsening airways resistance or lung/chest wall compliance results in increases in peak inspiratory pressure with continued delivery of set tidal volume (unless peak pressure limit is exceeded).

Time-cycled breath (pressure control breath)

This type of breath applies a constant pressure for a preset time. The constant pressure throughout inspiration produces a square pressure over time waveform during inspiration and a decelerating inspiratory flow waveform as the pressure gradient falls between the ventilator (pressure remains constant) and the patient (pressure rises as the lung fills). With this type of breath, changes in airway resistance or lung/chest compliance will alter tidal volume (i.e. worsening of airways resistance or lung compliance results in a decrease in tidal volume).

Flow-cycled breath (pressure support breath)

This type of breath is very similar to a time cycled breath in that a constant pressure is applied throughout inspiration and the inspiratory flow waveform is decelerating. The difference is only in the cycling mechanism. Pressure support breaths are terminated when the flow rate decreases to a predetermined percentage of the initial flow rate (typically 25%). Termination of the patient's inspiratory effort decreases flow, which markedly influences the end of inspiration.

Modes of ventilation (Table 3)

When mechanical ventilation is initiated, the optimum ventilatory support for a given clinical circumstance and the specific needs of the patient must be considered. A trial of non-invasive positive pressure ventilation (NPPV) may be considered in some circumstances (Pilbeam 2006).

Basically there are three breath delivery techniques: CMV, SIMV and spontaneous.


These modes are achieved by using some combination of the three types of ventilator breaths previously described. They may be combined with the application of positive end-expiratory pressure (PEEP). In choosing a mode, it is important to consider specific goals of ventilation:

* Adequacy of ventilation and oxygenation.

* A reduction of the work of breathing and the assurance of patient comfort and synchrony with the ventilator.

Controlled mechanical ventilation

CMV delivers mandatory ventilator breaths at a preset rate with either volume-cycled or time-cycled breaths. All breaths are mechanical ventilator breaths delivered by applications of position pressure to the airways. The patient is not able to initiate any additional ventilator breaths between the set controlled breaths. This mode can be achieved only in patients who are not capable of spontaneous respiratory effect (i.e. heavily sedated or receiving neuromuscular blockers). Resting the respiratory muscles allows redistribution of blood flow and better delivery to other vital organ systems.

Assist-control ventilation also delivers either volume-cycled or time-cycled breaths. A preset tidal volume (Vt) (volume ventilation) or preset applied pressure and time (pressure control ventilation (PCV)) are delivered at a preset minimum rate. Additional ventilator breaths are delivered if the patient initiates inspiration. Therefore, the patient receives a minimum number of ventilator breaths synchronised to spontaneous effort (if present) and can increase that number--and therefore ventilatory support--on demand. Ventilator and patient must be in synchrony in this mode of ventilation otherwise work of breathing may be significantly increased.

Synchronised intermittent mandatory ventilation

SIMV delivers either volume-cycled or time-cycled breaths at a preset mandatory number each minute. Unlike assist/control ventilation, no additional ventilator breaths are possible. Patients may, however, initiate spontaneous breaths with whatever Vt they can generate. Since there may be episodes during which the patient is in various phases of spontaneous breathing when the machine is set to deliver a preset Vt, the use of synchronisation allows for enhanced patient-ventilator interaction by delivering the preset machine breath in conjunction with the patient's inspiratory effort. When no effort is sensed, the ventilator delivers the preset Vt at an interval that depends on the set rate. SIMV is almost always combined with pressure support ventilation (PSV) applied to the spontaneous breaths to augment spontaneous tidal volume. The selected level of pressure support should aim to offset endotracheal tube resistance (usually a level of 5-10cm [H.sub.2]O).

One advantage of the SIMV mode is that it allows patients to assume a portion of their ventilatory requirement. The negative inspiratory pressure generated by spontaneous breathing leads to increased venous return to the right side of the heart, which may improve cardiac output and cardiovascular function. SIMV would essentially become CMV if the patient does not initiate spontaneous breaths.

Spontaneous ventilation

There are three basic means of providing spontaneous breathing during mechanical ventilation: Spontaneous, Pressure Support Ventilation (PSV) and Continuous Positive Airway Pressure (CPAP).

Patients can breathe effectively through a ventilator circuit utilising the endotracheal tube (ET) and humidified oxygen. The ventilator can monitor the patient's respiratory function and activate alarms if parameters are not achieved. The down side is that circuits require considerable effort to open inspiratory valves to allow gas flow, causing increased work of breathing.

PSV provides a preset level of inspiratory pressure assist with each breath. All breaths are flow-cycled. This inspiratory assist is selected to overcome the increased work of breathing imposed by the disease process, ET, the inspiratory valves and other mechanical aspects of ventilatory support. The pressure support applied augments each patient-generated breath. With PSV, the patient controls the respiratory rate and exerts a major influence on the duration of the inspiration, inspiratory flow rate and the Vt. Pulmonary compliance and resistance influence the delivered Vt. Rapid changes in these parameters will, therefore, potentially alter the minute ventilation and work requirements for the patient.

The amount of pressure support set during mechanical ventilation is titrated according to the Vt exhaled by the patient. Suggested parameters include a pressure-support setting that achieves one or more of the following goals:

* A Vt 6-10mL/Kg, depending on patient needs.

* A slowing of spontaneous breathing rate to an acceptable range.

* The desired minute ventilation.

Absent patient respiratory effort leads to the absence of any ventilatory support if PSV is used in insolation. A back-up ventilation setting is therefore required in case of apnoea and is standard on many mechanical ventilators. PSV may reduce the work of breathing by enhancing patient-ventilator interaction. Typically, as pressure support is increased in patients with lung disease, the patient's work of breathing and respiratory rate decrease, and Vt increases.

CPAP can be useful in improving oxygenation in patients with refractory hypoxemia related to acute lung injury. CPAP applies pressures above ambient to improve oxygenation in the spontaneously breathing patient. Used in conjunction with PEEP, airways are theoretically prevented from alveolar collapse at the end of expiration by increasing the functional residual capacity of the lungs. It is important to note that CPAP and PEEP aim to improve oxygenation, not provide ventilation.

A hybrid of CPAP/PEEP therapy is BiPAP, a patient triggered, pressure targeted and flow or time cycled form of ventilation, using an inspiratory pressure higher than the expiratory pressure.

Initial ventilator settings

When initiating ventilatory support in adults an inspired oxygen (Fi[O.sub.2]) level of 0.5-1.0 is used to ensure maximal amounts of available oxygen during the patient's adjustment to the ventilator and during the initial attempts to stabilise the patient's condition (Pilbeam 2006).

The usual recommendations for Vt are 8-10mL/kg. Higher Vt should be avoided to diminish the possibility of pulmonary barotrauma or volutrauma (Petrucci & Lacovelli 2004). An appropriate respiratory rate (RR) (10-15 breaths/min) for the desired minute ventilation should be chosen. Normal minute ventilation (MV = Vt x RR) is approximately 6-12 L/min. MV should be titrated to produce the PaC[O.sub.2] level that allows the appropriate acid/base (pH) status for the patient's clinical condition. As a general rule, Fi[O.sub.2], mean airway pressure and PEEP affect the Pa[O.sub.2] and RR, dead space and Vt affect alveolar minute ventilation and PaC[O.sub.2].

Continuing care during mechanical ventilation

Many important interrelationships exist among ventilator settings, and the consequences of making any change must be appreciated. This interdependency may lead to effects that are beneficial or harmful to the lung or cardiovascular system.

Inspiratory pressure

During positive pressure ventilation, airway pressure rises progressively to a peak pressure (PIP) that is reached at end-inspiration. This pressure is the sum of two pressures: the pressure required to overcome airway resistance and the pressure required to overcome elastic properties of the lung and chest wall. The pressure at the end of inspiration with airway closed, reflects the best estimate of peak alveolar pressure, which is an important indicator of alveolar distension. Accurate measurement of PIP requires the absence of any patient effort during inspiration or expiration.

Potential adverse effects from high inspiratory pressure include barotrauma (pneumothorax, pneumomediastinum), volutrauma (lung parenchymal injury due to over-inflation), and reduced cardiac output.

Interventions to assist in reducing an elevated PIP include reducing PEEP (this may also decrease oxygenation) and decreasing Vt (this may lead to hypercapnia due to reduction in MV). Permissive hypercapnia should not be used in patients with elevated intra-cranial pressure, as hypercapnia may increase cerebral blood flow and cerebral blood volume and further elevate ICP.

Inspiratory time: expiratory time relationship (I:E ratio)

The total respiratory cycle is 60 seconds divided by the respiratory rate. The times for inspiratory and expiratory occur within the total cycle and are related as the I:E ratio. During spontaneous breathing, the normal I:E ratio is 1:2. However, in chronic lung disease and other conditions associated with expiratory flow limitations, the exhalation time becomes prolonged and the I:E ratio changes (1:2.5, 1:3). These changes are reflective of lung disease pathophysiology and play an important role in deciding which ventilatory technique is best suited to the individual patient.

The inspiratory time in AC or SIMV mode is usually determined by the Vt and inspiratory gas flow rate. A larger Vt takes longer to deliver at the same flow rate, and the same Vt takes longer to deliver at a slower flow rate. In both cases the inspiratory time is longer but, at a constant respiratory rate, the cycle time remains the same. Therefore, the inspiratory time is 'actively' set by adjusting Vt and inspiratory flow rate, and expiratory time, however, is passively determined (i.e. 'what is left over' in cycle time before next inspiratory cycle of the ventilator or spontaneous breath).

If expiratory time does not allow full exhalation, the next lung inflation will be delivered upon the residual gas in the lung. This will result in hyperinflation and the development of PEEP, above the preset level of ventilator PEEP. This increase in end-expiratory pressure is called auto-PEEP. The potentially harmful physiologic effects of auto-PEEP on airway pressures, lung injury or cardiovascular function are the same as for preset PEEP. Effective interventions to reduce the effect of auto-PEEP include reducing RR, Vt or inspiratory time. Resultant effect on PaC[O.sub.2], pH and MV must be considered.

Inspired oxygen (Fi[O.sub.2])

Inspired oxygen may be harmful to the lung parenchyma after prolonged exposure. Although the precise threshold for concern is not known, it is desirable to aim for a Fi[O.sub.2] to [less than or equal to] 0.5 as soon as possible. However hypoxemia should always be considered a greater risk to the patient that high Fi[O.sub.2] levels.

The primary determinants of oxygenation during mechanical ventilation are the Fi[O.sub.2] and mean airway pressure (Paw). In the patient with acute lung injury, PEEP becomes an additional independent determinant. The interrelationships of these various parameters often lead to complex adjustments within the plan for mechanical ventilation.

Minute ventilation

The primary determinant of C[O.sub.2] exchange during mechanical ventilation is alveoli minute ventilation, calculated as Vt less dead space x RR. The physiological effect of high amounts of dead space is alveolar that are relatively well ventilated but underperfused, resulting in hypercapnia. This may result from the pathologic process in the lung or from mechanical ventilation complicated by high airway pressures, low intravascular volume or low cardiac output. If hypercapnia persists during mechanical ventilation, consultation with an intensivist should be sought. It may be necessary to use a low Vt to avoid high airway pressures and/or a low respiratory rate to avoid auto-PEEP, thus permitting hypoventilation and hypercapnia.

Adequate ventilation is assessed by consideration of both the PaC[O.sub.2] and the pH. Hyperventilation resulting in a low PaC[O.sub.2] level may be an appropriate short-term compensatory goal during metabolic acidosis while the primary aetiology is corrected. Similarly, a patient with chronic hypercapnia has a baseline increased PaC[O.sub.2] and maintains a near-normal pH by renal compensation (retention of bicarbonate). Patients with chronic compensated hypercapnia should receive sufficient minute ventilation during mechanical ventilation to maintain the PaC[O.sub.2] at the patient's usual level to avoid severe alkalaemia and loss of retained bicarbonate.

Sedation, analgesia and neuromuscular blockade

All situations where a patient requires mechanical ventilation, whether it is planned (for example, elective major surgery or unplanned, for example, acute respiratory arrest) causes stress and anxiety. To improve patient comfort, help relieve anxiety and reduce the patient's work of breathing, anxiolytics, sedatives, analgesics and neuromuscular blockade agents are frequently administered. Guidelines for the use of these agents would relate to specific intensive care unit policy. Caution should be taken with the use of sedation in the non-intubated patient who has acute respiratory insufficiency or impending respiratory failure.

Monitoring mechanical ventilatory support

Patients who receive mechanical ventilatory support required continuous monitoring to assess the beneficial and adverse effects of treatment. Positive pressure ventilation affects not only the respiratory status of the patient but also their cardiovascular, renal and vascular systems. The following monitoring should be done as routine:

* Intermittent measurement of vital signs (BP, HR, urine output, arterial blood gases). Hypotension, tachycardia, hypovolemia, decreased urine output and increased metabolic acidosis are signs of a decreased cardiac output (CO) and venous return (VR). During positive pressure ventilation inspiration, intrathoracic pressure increases resulting in decreased VR, increased RV afterload and thus decreased LV output. PEEP may further reduce VR. Anxiety and distress prior to initiation of ventilation and the use of sedation may also have an effect on peripheral vascular tone.

* Urine output. A reduction in cardiac output activates the release of anti-diuretic hormone (ADH) and stimulation of the renin-angiotensin-aldosterone (RAA) response, resulting in sodium and water retention in the body. This is manifested in a decreased urine output.

* Respiratory function observations (patient/ventilator synchronisation, chest auscultation, airway (patency, secretions, pressures), breathing (rate, volume, oxygenation), arterial blood gas (ABG) measurements, chest radiography (CXR). Continuous monitoring allows for confirmation of tube position and oxygenation response of ventilatory changes to be observed almost immediately. Lung compliance may increase pressures, particularly where bronchoconstriction increases resistance to flow and significantly increases airway pressures. Lung damage may show clinically as a pneumothorax or pneumomediastinum. The normal humidification and air-warming mechanisms of the upper airways are bypassed when a patient is intubated. This combined with the delivery of dry, cool gases has deleterious effects on the trachea and bronchi. Ciliary function is depressed and increased thickened mucus can cause inflammation and microatelectasis. The intubated patient has a reduced ability to cough and clear secretions, therefore regular bronchial suctioning is required to reduce the risk of atelectasis and shunting and to ensure tube patency.

* Maintaining communication. Patients already have an increased level of stress and anxiety and this is compounded by their inability to communicate and respond. Explanation and reassurance is essential and should be undertaken, regardless of whether the patient is fully sedated.

* Nutritional status. Maintaining an accurate fluid balance document is essential. As patients are unable to take an oral diet, enteral or parenteral feeding regimes need to be established early to maintain nutritional status and reduce the depletion of minerals and trace elements important for respiratory muscle function.

* Infection risk. Ventilation associated pneumonia is a well-documented complication of mechanical ventilation (Jackson 2006, Tolentino-Delos Reyes 2007). Maintenance of aseptic principles in suctioning technique and ensuring ET cuff seal is vital to avoid potential bacterial colonisation.

Complications of mechanical ventilation

Although mechanical ventilation may be a life-saving intervention, it also presents numerous potential complications. These are listed in Table 4. These complications can be avoided or reduced with careful management and close monitoring of the clinical condition of the patient and responding promptly to presenting problems.


This article reviews the basic concepts that are fundamental to an understanding of mechanical ventilation. Instituting a mechanical ventilatory strategy requires a complex interaction of modes, techniques and continual monitoring and adjustment by experienced clinicians. A working knowledge of indications, selection of mode (CMV, SIMV, Spontaneous) and initial settings (breath, volumes, pressures) is essential. Understanding these principles helps to fine tune the ventilator parameters to accommodate the needs of the patient.

For practitioners new to the management of mechanical ventilation, clinical exposure and mentoring by an experienced critical care nurse are invaluable for learning when ventilation is necessary and how techniques can be manipulated to ensure optimal benefit and comfort for the patient.

Provenance and Peer review: Commissioned by the Editor; Peer reviewed.

Task 1


Review respiratory physiology and reflect on how your new knowledge will improve your practice and patient care.


Notional Learning Hours

1 hour for your reflection.

Knowledge and Skills Dimension

Core 2: Personal and people development.

Task 2


Review oxygenation and acid-base evaluation and reflect on how your new knowledge will improve your practice and patient care.


Notional Learning Hours

1 hour for your reflection.

Knowledge and Skills Dimension

Core 2: Personal and people development.

Task 3

Spend some time supernumerary in ICU working with an experienced nurse caring for a ventilated patient. Use this experience as the basis for a scheme of work.


1. Review this article in relation to your experience.

2. Complete a case study on one of your experiences.

3. Reflect on your experience and what knowledge you will bring to your existing role.

Notional Learning Hours


1 hour for the review.

1 hour for your case study.

1 hour for your reflection.

Knowledge and Skills Dimension

1. Review

Core 2: Personal and people development.

2. Case Study

Core 3: Health, safety and security

Health and wellbeing HWB6: Assessment and treatment planning

Level 3: Assess physiological and psychological functioning and develop, monitor and review related treatment plans.

Health and wellbeing HWB7: Interventions and treatments.

Level 4: Plan, deliver and evaluate interventions and/or treatments when there are complex issues and/or serious illness.

3. Reflection

Core 2: Personal and people development.

Task 4


Explore your department and see how many types of ventilators you use on a day to day basis. Describe their mode of action.

Notional Learning Hours


1 hour to complete your project. For an example, this could become a poster presentation.

Knowledge and Skills Dimension

Core 1: Communication

Task 5


Reflect on how the care of the mechanically ventilated patient in ICU differs from that of the ventilated patient in theatre.

Notional Learning Hours


1 hour for your reflection.

Knowledge and Skills Dimension

Core 2: Personal and people development.

Associated AfPP online modules: Back to basics

All these modules will have Knowledge and Skills Framework dimensions and Notional Learning Hours Attached. To complete this learning resource go to the AfPP website and enter the Online Learning site which is under the Career Development tab.

* Airway Management

* Breathing Management

* Breathing Circuits and Their Uses

* Anaesthetic Drugs

* Supportive Pharmacology

* Circulation and Invasive Monitoring

Web links and key documents

Anaesthesia UK:

Virtual Anaesthesia Textbook:

World anaesthesia online:

Reflective model

You will find this reflective module template and many others under the career development tab on the AfPP website.

* What information do I need to access in order to learn from the experience?

* Five phases with cue questions:

Description of the experience.


Influencing factors.

Could I have dealt with the situation better? Learning.


Additional Learning Resources


Esteban A, Anzueto A, Alia I 2000 How is mechanical ventilation employed in the intensive care unit? American Journal of Respiratory Critical Care Medicine 161 (5) 1450-1458

Jackson WL, Shorr AF 2006 Update on ventilator-associated pneumonia Current Opinion in Anaesthesiology 9 (2) 117-121

Lassen HC 1953 A preliminary report on the 1952 epidemic of poliomyelitis in Copenhagen with special treatment of acute respiratory insufficiency Lancet 1 (1) 37-41

Petrucci N, Lacovelli W 2004 Ventilation with lower tidal volumes versus traditional tidal volumes in adults with acute lung injury and acute respiratory distress syndrome Cochrane Database Systematic Review (92): CD003844

Pilbeam SP, Cairo JM 2006 Mechanical Ventilation: Physiological and Clinical Applications (4th Edition) St Louis, Mosby

Tobin MJ 1994 Current Concepts: Mechanical Ventilation New England Journal of Medicine 330 (15) 1056-1061

Tobin MJ 2001 Medical progress: advances in mechanical ventilation New England Journal of Medicine 344 (26) 1986-1996

Tolentino-Delos Reyes AF, Ruppert SD, Shiao SY 2007 Evidence-based practice: use of the ventilator bundle to prevent ventilator-associated pneumonia American Journal of Critical Care 16 (1) 20-27

Correspondence address: Catherine Carbery, Clinical Nurse Manager/Acting Nurse Coordinator, Intensive Care, Royal Melbourne Hospital, Grattan Street, Parkville 3050, Victoria, Australia.

Catherine Carbery

Clinical Nurse Manager/Acting Nurse Coordinator, Intensive Care, Royal Melbourne Hospital
Table 1 Physiological and clinical objectives of mechanical

1. Support or manipulate pulmonary gas exchange

* Alveolar ventilation--achieve normal or allow permissive
hypercapnia (n.b. permissive hypercapnia sometimes is required in
the ventilation of patient with asthma, acute lung injury (ALI), or
acute respiratory distress syndrome (ARDS) to avoid high
ventilating volumes and pressures).

* Alveolar oxygenation--maintain oxygen delivery (Ca[O.sub.2] x
Cardiac Output) at or near normal.

2. Increase lung volume

* Prevent or treat atelectasis with adequate end-inspiratory lung

* Restore and maintain an adequate functional residual capacity

3. Reduce the work of breathing (WOB)

Clinical objectives

1. Reverse acute respiratory failure.

2. Reverse respiratory distress.

3. Reverse hypoxemia.

4. Prevent or reverse atelectasis and maintain FRC.

5. Reverse respiratory muscle fatigue.

6. Permit sedation or paralysis (or both).

7. Reduce systemic or myocardial oxygen consumption.

8. Minimise associated complications and reduce mortality.

Table 2 Indications for invasive mechanical ventilation in adults
with acute respiratory failure

Invasive mechanical ventilation is indicated in any of the
following circumstances:

1. Apnoea or impending respiratory arrest

2. Acute exacerbation of chronic obstructive pulmonary disease
(COPD)* with dyspnoea, tachypnoea, and acute respiratory acidosis
(hypercapnia and decreased arterial pH) plus at least one of the

* Acute cardiovascular instability

* Altered mental status or persistent uncooperativeness

* Inability to protect the lower airway

* Copious or unusually viscous secretions

* Abnormalities of the face or upper airway that would prevent
effective non-invasive positive pressure ventilation

3. Acute ventilatory insufficiency in cases of neuromuscular
disease accompanied by any of the following:

* Acute respiratory acidosis (hypercapnia and decreased arterial

* Progressive decline in vital capacity to below 10-15mL/kg

* Progressive decline in maximum inspiratory pressure to below -20
to -30cm [H.sub.2]O

4. Acute hypoxaemic respiratory failure with tachypnoea,
respiratory distress and persistent hypoxaemia despite
administration of a high fraction of inspired oxygen (Fi[O.sub.2])
with high-flow oxygen devices or in the presence of any of the

* Acute cardiovascular instability

* Altered mental status or persistent uncooperativeness

* Inability to protect the lower airway

5. Need for endotracheal intubation to maintain or protect the
airway or to manage secretions, given the following factors:

* Endotracheal tube (ETT) [less than or equal to] 7mm with minute
ventilation >10L/min

* ETT [less than or equal to] 8mm with minute ventilation >15 L/min

If the conditions listed previously are not factors, emergency
intubation and invasive positive pressure ventilation may not be
indicated for the following conditions until other therapies have
been attempted:

* Dyspnoea, acute respiratory distress

* Acute exacerbation of COPD

* Acute severe asthma

* Acute hypoxaemic respiratory failure in immunocompromised

* Hypoxaemia as an isolated finding

* Traumatic brain injury

* Flail chest

Modified from Pierson DJ 2003 Indications for mechanical
ventilation in adults with acute respiratory failure Respiratory
Care 47 (2) 249. *Applicable to acute severe asthma if respiratory
acidosis or airflow obstruction worsens despite aggressive
management with bronchodilators and other therapy.

Table 3 Modes of ventilation

Ventilatory Modes

Mode                    Description             Clinical Use

Controlled mechanical   [a] pre-set TV and      Patient requires
ventilation (CMV):      frequency of breaths    complete mechanical
[a] volume-controlled   delivered               ventilatory support.
[b] pressure-           [b] breaths
controlled              delivered to preset
                        pressure with TV
                        varying with lung

Assist/Control (AC)     Preset TV breaths       Patient able to
(triggered)             delivered in response   initiate breaths but
                        to patient attempting   requires ventilatory
                        spontaneous breath.     assistance to
                        Back-up delivers        maintain oxygenation
                        preset rate of          and C[O.sub.2]
                        breaths if patient      removal.
                        does not achieve set

Synchronised            Preset TV breaths       Patient being weaned
intermittent            delivered at preset     from ventilation or
mandatory               rate but spontaneous    for greater patient
ventilation (SIMV)      breaths allowed in      comfort/reduction of
                        between and             sedation
                        ventilator breaths      requirements.
                        synchronised with
                        spontaneous breaths.

Pressure support        Following triggering    Patient being weaned
(PSV)                   by patient, breath is   from ventilation or
                        delivered to preset     for greater patient
                        pressure level, TV      comfort/reduction of
                        delivered will          sedation
                        depend on lung          requirements.

Spontaneous             Patient triggered       Patient being weaned
                        and controlled.         from ventilation or
                                                for greater patient
                                                comfort/ reduction
                                                of sedation

TV = Tidal Volume

Table 4 Complications of mechanical ventilation

Equipment         Malfunction or disconnection
                  Incorrect parameters set or prescribed
                  Contamination of ventilator or circuit

Pulmonary         Damage to structures during airway intubation
                  (teeth, trachea, vocal cords)
                  Ventilator-associated pneumonia reducing lung
                  Diffuse lung injury related to over-distension,
                  alveolar rupture, inadequate PEEP
                  Barotrauma (pneumothorax)
                  Oxygen toxicity
                  Asynchrony between patient and ventilator
                  Muscle weakness

Cardiovascular    [down arrow] RV preload [down arrow] cardiac output
                  [up arrow] RV afterload (over-distension)
                  [up arrow] ICP with high PEEP
                  Fluid retention due to [down arrow] cardiac
                  output and [down arrow] renal blood flow

GIT               Distension
                  Mucosal ulceration

Neurological      Sleep disturbances, agitation, discomfort
                  Neuropsychosis complications
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