Oxford Handbook of Critical Care - part 1 doc

N Engl J Med 2000; 342:1301–8 See also: IPPV—modes of venti lation, p8; IPPV—adjusti ng the venti lator, p10; IPPV—failure to tol erate ventil ation, p12; IPPV—compli cations of venti la

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Andrew R

Critical Care, 2nd Edition

A R Webb

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P.4

Ovid: Oxford Handbook of Critical Care

Editors: Singer, Mervyn; Webb, Andrew R.

Title: Oxford Handbook of Critical Care, 2nd Edition

> Table of Co ntents > Respirator y Therapy Tech niques

Respiratory Therapy Techniques

Oxygen therapy

All criticall y i ll patients should recei ve additi onal inspired oxygen on a ‘more not less i s best’ phi losophy.

Principles

High flow, high concentrati on oxygen shoul d be given to any acutely dyspnoei c or hypoxaemic patient until accurate

ti tration can be performed usi ng arterial bl ood gas anal ysi s

In general, mai ntain SaO2 >90%, though preferabl y >95% Compromi ses may need to be made duri ng acute on

chroni c hypoxaemic respi ratory fail ure, or prol onged severe ARDS, when lower values may suffi ce provided tissue

oxygen del ivery is maintained

Al l pati ents placed on mechanical ventilati on should initi all y receive a high FIO2 until accurate titrati on is performed

usi ng arterial bl ood gas anal ysi s

Apart from pati ents receiving hyperbaric O2 therapy (e.g for carbon monoxide poi soning, diving accidents), there is

no need to maintai n supranormal l evels of PaO2

Cautions

A small proportion of pati ents i n chronic Type II (hypoxaemi c, hypercapnic) respi ratory fail ure wi ll develop apnoea i f

their central hypoxi c drive i s removed by suppl emental oxygen However, thi s i s seldom (if ever) abrupt and a period

of deteri orati on and increasi ng drowsi ness will al ert medi cal and nursing staff to consi der ei ther (i) FIO2 reduction if

overal l condition al lows, (ii ) non-i nvasi ve or i nvasi ve mechani cal venti lation i f fati gui ng or (ii i) use of respi ratory

sti mulants such as doxepram The coroll ary i s that cl ose supervision and moni toring i s necessary in all criticall y i ll

patients

A normal pul se oxi metry readi ng may obscure deteriorating gas exchange and progressi ve hypercapnia

Oxygen toxicity is described in ani mal model s Normal volunteers wil l become symptomatic after several hours of

breathing pure oxygen Furthermore, washout of ni trogen may l ead to mi croatelectasis However, the relevance and

rel ative importance of oxygen toxi ci ty compared to other forms of ventilator trauma i n cri tical ly ill pati ents i s stil l far

from clear Efforts should neverthel ess be made to minimi se FIO2 whenever possi ble Debate continues as to whether

FIO2 or other ventil ator settings (e.g PEEP, VT, i nspiratory pressures) should be reduced fi rst The authors' present

view i s to mini mise the ri sks of ventil ator trauma

Monitoring

An oxygen analyser in the i nspiratory l imb of the ventil ator or CPAP/Bi PAP ci rcuit confi rms the pati ent is recei ving a

known FIO2 Most modern ventil ators have a bui lt-in calibration devi ce

Adequacy and changes in arteri al oxygen saturati on can be conti nuousl y moni tored by pul se oxi metry and

intermittent or continuous invasive bl ood gas anal ysi s

Oxygen masks

Hudson-type masks or nasal ‘spectacles’ gi ve an i mpreci se FIO2 and should onl y be used when hypoxaemia is not

a major concern Hudson-type masks do all ow del ivery of humi di fied gas (e.g via an ‘Aquapak’) Val ves fi tted tothe Aquapak system do not del iver an accurate FIO2 unless gas flow i s at the recommended l evel

Masks fitted with a Venturi val ve del iver a reasonably accurate FIO2 (0.24, 0.28, 0.35, 0.40, 0.60) except i npati ents with very hi gh inspiratory flow rates These masks do not all ow del ivery of humidi fied gas but arepreferabl e i n the short term for dyspnoeic patients as they enable more precise monitoring of PaO2/FIO2 rati os

A tight-fitting anaesthetic mask and reservoi r bag all ows 100% oxygen to be del ivered

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Defined by an acute rise in PaCO2 and a signi ficant respi ratory acidosi s PaCO2 is di rectl y proportional to the body's

CO2 producti on and inversel y proportional to al veol ar venti lation (minute ventil ati on minus dead space ventilation)

Causes include:

Respiratory centre depressi on, e.g depressant drugs or i ntracranial pathologyPeri pheral neuromuscular di sease, e.g Gui ll ain–Barré syndrome, myasthenia gravi s or spinal cord pathol ogyTherapeuti c muscle paral ysi s, e.g as part of balanced anaesthesia, for management of tetanus or statusepi lepticus

Loss of chest wall integrity, e.g chest trauma, di aphragm ruptureHigh CO2 production, e.g burns, sepsis or severe agitati on

Reduced al veolar venti lation, e.g ai rway obstructi on (asthma, acute bronchi ti s, foreign body), atel ectasi s,pneumonia, pulmonary oedema (ARDS, cardi ac fai lure), pl eural pathol ogy, fibroti c l ung di sease, obesi tyPul monary vascul ar di sease (pul monary embol us, cardi ac fai lure, ARDS)

Oxygenation failure

Hypoxaemi a i s defi ned by PaO2 <11kPa on FIO2≥0.4 May be due to:

Ventil ati on–perfusion mi smatching (reduced venti lation i n, or preferential perfusi on of, some l ung areas), e.g

pneumonia, pulmonary oedema, pul monary vascular di sease, extremel y high cardi ac outputShunt (normal perfusi on but absent venti lation i n some lung zones), e.g pneumonia, pulmonary oedemaDiffusion li mitati on (reduced alveol ar surface area wi th normal venti lation), e.g emphysema; reduced i nspiredoxygen tension, e.g alti tude, suffocati on

Acute ventil atory insuffici ency (as above)

To reduce intracranial pressure

Reduction of PaCO2 to approximately 4kPa causes cerebral vasoconstriction and therefore reduces intracranial

pressure after brain injury Recent studi es suggest this effect i s transi ent and may i mpair an already cri tical cerebral

blood flow

To reduce work of breathing

Assisted venti lation ± sedati on and muscl e relaxation reduces respi ratory muscl e acti vity and thus the work of

breathing In cardiac fail ure or non-cardiogeni c pulmonary oedema the resul ti ng reduction i n myocardi al oxygen

demand is more easily matched to the suppl y of oxygen

Indications for ventilatory support

Venti latory support (invasive or non-i nvasive) should be considered i f:

Respiratory rate >30/minVital capaci ty <10–15ml/minPaO2 <11kPa on FIO2≥0.4PaCO2 high wi th si gni ficant respiratory acidosi s (e.g pH <7.2)Vd/VT >60%

Qs/Qt >15–20%

ExhaustionConfusi onSevere shockSevere LVFRaised ICP

See also:

Dyspnoea, p278; Ai rway obstruction, p280; Respiratory fail ure, p282; Atel ectasi s and pul monary coll apse, p284;

Chroni c airflow l imi tation, p286; Acute chest i nfecti on (1), p288; Acute chest infection (2), p290; Acute respiratory

distress syndrome (1), p292; Acute respiratory distress syndrome (2), p294; Asthma—general management, p296;

Asthma—venti latory management, p298; Inhal ati on injury, p306; Pulmonary embol us, p308; Heart

fai lure—assessment, p324; Heart fail ure—management, p326; Acute li ver fai lure, p360; Acute weakness, p368;

Agi tation/confusi on, p370; Generalised sei zures, p372; Intracranial haemorrhage, p376; Subarachnoi d haemorrhage,

p378; Stroke, p380; Raised i ntracranial pressure, p382; Guill ain–Barré syndrome, p384; Myasthenia gravis, p386;

ICU neuromuscul ar disorders, p388; Tetanus, p390; Botul ism, p392; Poisoni ng—general principles, p452; Sedati ve

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poi soning, p458; Tricycl ic antidepressant poisoning, p460; Cocaine, p464; Inhaled poisons, p466; Organophosphate

poi soning, p472; Systemi c i nfl ammati on/mul ti-organ fai lure, p484; Multipl e trauma (1), p500; Multi pl e trauma (2),

p502; Head i njury (1), p504; Head injury (2), p506; Spi nal cord injury, p508; Burns—flui d management, p510;

Burns—general management, p512; Near-drowni ng, p526; Post-operative intensive care, p534

IPPV—description of ventilators

Classification of mechanical ventilators

These may be cl assifi ed by the method of cycli ng from i nspirati on to expi ration Thi s may be when a preset ti me has

elapsed (time-cycl ed), a preset pressure reached (pressure-cycl ed) or a preset vol ume delivered (vol ume-cycled)

Though the method of cycl ing i s classi fied accordi ng to a single constant, modern ventilators all ow a greater degree

of control In vol ume-cycled mode with pressure limitati on, the upper pressure alarm l imi t i s set or the maximum

inspi ratory pressure control led The ventil ator deli vers a preset tidal vol ume (VT) unless the lungs are non-compliant

or airway resistance is hi gh This is useful to avoid hi gh peak ai rway pressures In volume-cycl ed mode with a time

li mit, the inspiratory fl ow i s reduced; the ventil ator deli vers the preset VT unless impossibl e at the set respi ratory

rate If pressure li mitati on is not avail abl e thi s i s useful to limit peak airway pressures In time-cycled mode wi th

pressure control, preset pressure i s del ivered throughout inspi ration (unli ke pressure-cycled venti lation), cycli ng

bei ng determined by time VT i s dependent on respiratory compli ance and airway resistance Here, too, high peak

airway pressures can be avoided

Setting up the mechanical ventilator

Tidal volume

Conventional ly set at 7–10ml/kg, though recent data suggest l ower values (6–7ml /kg) may be better in severe acute

respi ratory failure, reducing barotrauma and improving outcome In severe airflow l imi tation (e.g asthma, acute

bronchitis) small er VT and minute volume may be needed to allow prol onged expiration

Respiratory rate

Usuall y set in accordance with VT to provi de mi nute venti lation of 85–100ml /kg/mi n In time-cycl ed or time-l imi ted

modes the set respiratory rate determi nes the ti mi ng of the ventil ator cycles

Inspiratory flow

Usuall y set between 40–80l/min A hi gher flow rate is more comfortabl e for alert patients This all ows for l onger

expirati on i n patients with severe airflow l imi tation but may be associ ated wi th hi gher peak ai rway pressures The

flow pattern may be adjusted on most ventil ators A square waveform is often used but decelerating fl ow may reduce

peak airway pressure

I:E ratio

A functi on of respiratory rate, VT, inspi ratory fl ow and inspi ratory ti me Prolonged expi ration is useful i n severe

airfl ow l imitation whil e a prolonged i nspiratory time i s used in ARDS to all ow slow reacting alveoli ti me to fil l Al ert

patients are more comfortable with shorter i nspiratory times and high i nspiratory flow rates

FIO2

Set accordi ng to arteri al blood gases Usual to start at FIO2=0.6–1 then adjust according to arterial blood gases

Airway pressure

In pressure-controll ed or pressure-li mited modes the peak airway pressure (ci rcuit rather than al veol ar pressure) can

be set (usually ≤35–40cmH2O) PEEP is usual ly increased to maintai n FRC when respi ratory compl iance is low

Initial ventilator set-up

Check for leaks

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Key trial

Acute Respiratory Di stress Syndrome Network Venti lation wi th lower ti dal volumes compared with traditi onal tidal

vol umes for acute lung i njury and the acute respiratory distress syndrome N Engl J Med 2000; 342:1301–8

See also:

IPPV—modes of venti lation, p8; IPPV—adjusti ng the venti lator, p10; IPPV—failure to tol erate ventil ation, p12;

IPPV—compli cations of venti lation, p14; IPPV—weaning techniques, p16; IPPV—assessment of weaning, p18; Hi gh

frequency venti lation, p20; Positive end expiratory pressure (1), p22; Positive end expi ratory pressure (2), p24; Lung

recruitment, p28; Non-invasive respi ratory support, p32; CO2 moni toring, p92; Bl ood gas anal ysi s, p100

IPPV—modes of ventilation

Controlled mechanical ventilation (CMV)

A preset number of breaths are delivered to supply all the pati ent's venti latory requi rements These breaths may be

at a preset VT (volume control led) or at a preset i nspiratory pressure (pressure controll ed)

Assist control mechanical ventilation (ACMV)

Patients can trigger the ventilator to determine the respiratory rate but, as wi th CMV, a preset number of breaths are

del ivered i f the spontaneous respiratory rate fall s below the preset level

Intermittent mandatory ventilation (IMV)

A preset mandatory rate is set but pati ents are free to breathe spontaneously between set ventil ator breaths

Mandatory breaths may be synchroni sed wi th patients' spontaneous efforts (SIMV) to avoid mandatory breaths

occurring duri ng a spontaneous breath This effect, known as ‘stacking’ may lead to excessive ti dal volumes, hi gh

airway pressure, i ncompl ete exhal ati on and ai r trappi ng Pressure support may be added to spontaneous breaths to

overcome the work of breathi ng associ ated with openi ng the venti lator demand valve

Pressure support ventilation (PSV)

A preset inspi ratory pressure i s added to the ventil ator circui t duri ng inspi ration in spontaneously breathing patients

The preset pressure should be adjusted to ensure adequate VT

Choosing the appropriate mode

Pressure controll ed ventil ati on avoids the dangers associated with high peak airway pressures, although it may resul t

in marked changes in VT if compli ance alters Allowing the patient to make some spontaneous respiratory effort may

reduce sedation requi rements, retrain respi ratory muscl es and reduce mean airway pressures

Apnoeic patient

Use of IMV or ACMV in patients who are totall y apnoeic provi des the total minute vol ume requi rement if the preset

rate i s high enough (thi s i s effecti vel y CMV) but allows spontaneous respiratory effort on recovery

Patient taking limited spontaneous breaths

A guaranteed mi nimum minute volume i s assured wi th both ACMV and IMV depending on the preset rate The work of

spontaneous breathing is reduced by suppl ying the preset VT for spontaneousl y triggered breaths with ACMV, or by

adding pressure support to spontaneous breaths with IMV Wi th ACMV the spontaneous tidal vol ume is guaranteed

whereas with IMV and pressure support spontaneous tidal volume depends on l ung compl iance and may be less than

the preset tidal vol ume The advantage of IMV and pressure support is that gradual reducti on of preset rate, as

spontaneous effort increases, all ows a smooth transiti on to pressure support ventil ati on Subsequent weaning i s by

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reduction of the pressure support l evel

See also:

IPPV—descri pti on of ventil ators, p6; IPPV—adjusti ng the venti lator, p10; IPPV—failure to tol erate ventil ation, p12;

recruitment, p28; Non-invasive respi ratory support, p32

IPPV—adjusting the ventilator

Venti lator adjustments are usual ly made i n response to bl ood gases, pulse oximetry or capnography, patient agitati on

or discomfort, or during weani ng ‘Migration’ of the endotracheal tube, ei ther distall y to the carina or beyond, or

proximall y such that the cuff is at vocal cord l evel, may resul t i n agi tation, excess coughi ng and a deteri oration i n

blood gases This, and tube obstruction, should be consi dered and recti fied before changi ng ventil ator or sedation

dose settings

The choice of ventilator mode depends upon the level of consciousness, the number of spontaneous breaths being

taken, and the blood gas val ues The spontaneousl y breathi ng patient can usuall y cope adequately with pressure

support ventil ati on alone However, on occasi on, a few intermittent mandatory breaths (SIMV) may be necessary to

assist gas exchange or slow an excessive spontaneous rate The paralysed or heavil y sedated patient wil l require

mandatory breaths, ei ther volume- or pressure-controll ed

The order of change wi ll be di ctated by the severity of respi ratory fail ure and i ndi vidual operator preference Earl ier

use of increased PEEP is advocated to recruit collapsed alveoli and thus improve oxygenati on in severe respi ratory

fai lure

Increase FIO2Revi ew VT and respiratory rateIncrease PEEP (may rai se peak ai rway pressure or reduce CO)Increase I:E ratio

Increase pressure support/pressure controlCMV, increase sedation ± muscle relaxantsConsider tol erating l ow level (‘permissive hypoxaemi a’)Prone ventil ati on, inhal ed nitri c oxide

Decrease l evel of pressure control/pressure support i f VT adequateDecrease PEEP

Decrease FIO2Decrease I:E ratio

Increase VT (if low and peak ai rway pressure allows)Increase respiratory rate

Reduce rate i f too high (to reduce intri nsi c PEEP)Reduce dead space

CMV, increase sedation ± muscle relaxantsConsider tol erating high level (‘permissi ve hypercapni a’)

Decrease respiratory rateDecrease VT

See also:

IPPV—descri pti on of ventil ators, p6; IPPV—modes of venti lation, p8; IPPV—fail ure to tolerate venti lation, p12;

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P.13P.14

recruitment, p28; Non-invasive respi ratory support

IPPV—failure to tolerate ventilation

Agi tation or ‘fighti ng the venti lator’ may occur at any time Poor tolerance may also be i ndi cated by hypoxaemi a,

hypercapnia, venti lator al arms or cardiovascular i nstabili ty

Poor gas exchange during initial phase of ventilation

Increase FIO2 to 1.0 and start manual venti lation

Check endotracheal tube i s correctly positioned and both lungs are being inflated Consider tube replacement,intratracheal obstructi on or pneumothorax

Check ventilator ci rcuit i s both intact and patent and venti lator is functioning correctly Check ventil ator settingsincluding FIO2, PEEP, I:E ratio, set tidal vol ume, respiratory rate and/or pressure control Check ‘pressure li mi t’

settings as these may be set too l ow, causi ng the venti lator to time-cycl e prematurel y

Poor tolerance after previous good tolerance

If agi tation occurs in a pati ent who has previousl y tolerated mechani cal venti lation, either the pati ent's condi tion has

deteri orated or there i s a probl em i n the venti lator circuit (including artifi cial airway) or the ventilator itsel f

The patient should be removed from the venti lator and pl aced on manual ventil ati on with 100% oxygen whil e theproblem i s resolved Resorting to increased sedation ± muscl e relaxation in this ci rcumstance i s dangerous untilthe cause is resol ved

Check patency of the endotracheal tube (e.g wi th a suction catheter) and re-i ntubate i f i n doubt

Consider malposi ti on of the endotracheal tube (e.g cuff above vocal cords, tube ti p at cari na, tube in mai nbronchus)

Seek and treat and changes i n the patient's condi ti on, e.g tension pneumothorax, sputum pl ug, pain

Where pati ents are making spontaneous respi ratory effort consider increasing pressure support or addi ngmandatory breaths

If pati ents fai l to synchronise with IMV by stacking spontaneous and mandatory breaths, increasi ng pressuresupport and reduci ng mandatory rate may hel p; alternati vel y, the use of PSV may be appropriate

See also:

IPPV—descri pti on of ventil ators, p6; IPPV—modes of venti lation, p16; IPPV—adjusting the ventilator, p10;

recruitment, p28; Non-invasive respi ratory support, p32; Sedatives, p238; Muscl e relaxants, p240;

Agi tation/confusi on, p370

IPPV—complications of ventilation

Haemodynamic complications

Venous return is dependent on passi ve flow from central veins to right atrium As right atrial pressure increases

secondary to the transmi tted i ncrease in intrathoraci c pressure across compl iant lungs, there is a reduction in venous

return Thi s i s l ess of a problem i f l ungs are sti ff (e.g ARDS) although i t wil l be exacerbated by the use of inverse

I:E ratio and high PEEP As lung vol ume is increased by IPPV the pulmonary vascul ature is constricted, thus

increasi ng pul monary vascular resistance This wi ll increase di astoli c volume of the ri ght ventricl e and, by septal

shi ft, i mpedes fil li ng of the left ventri cle These effects al l contribute to a reduced stroke vol ume This reduction can

be minimi sed by reducing ai rway pressures, avoi ding prol onged inspiratory ti mes and maintai ning blood volume

Ventilator trauma

The term barotrauma relates to gas escape into cavi ties and intersti tial tissues duri ng IPPV Barotrauma i s a

misnomer si nce it is probably the distending volume and high shear stress that i s responsible rather than pressure It

is most l ikely to occur wi th high VT and hi gh PEEP It occurs in IPPV and condi ti ons associated with l ung overi nfl ati on

(e.g asthma) Tension pneumothorax i s l ife threatening and should be suspected in any pati ent on IPPV who becomes

suddenly agi tated, tachycardi c, hypotensi ve or exhi bi ts sudden deteriorati on in their bl ood gases An i mmediate chest

drainage tube should be inserted if tensi on pneumothorax develops Preventi on of ventil ator trauma rel ies on

avoidance of hi gh VT and hi gh airway pressures

Nosocomial infection

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Endotracheal i ntubation bypasses normal defence mechanisms Cil iary activi ty and cellular morphology in the

tracheobronchi al tree are altered The requi rement for endotracheal suction further i ncreases susceptibil ity to

infection In addi ti on, the normal heat and moisture exchanging mechanisms are bypassed requi ri ng artifi ci al

humidi fi cation of inspi red gases Fail ure to provi de adequate humi di ficati on increases the risk of sputum retention

and infection Mai ntaini ng venti lated patients at 30° upright head til t has been shown to reduce the incidence of

nosocomial pneumonia

Acid–base disturbance

Venti lating patients wi th chronic respiratory fai lure or hyperventilation may, by rapid correcti on of hypercapnia,

cause respi ratory al kal osi s Thi s reduces pulmonary blood flow and may contri bute to hypoxaemia A respiratory

aci dosis due to hypercapni a may be due to i nappropriate ventilator setti ngs or may be desi red in an attempt to avoi d

high VT and ventil ator trauma

Water retention

Vasopressin released from the anterior pi tui tary i s increased due to a reduction i n i ntrathoraci c blood volume and

psychological stress Reduced urine fl ow thus contributes to water retenti on In addition, the use of PEEP reduces

lymphatic fl ow with consequent peripheral oedema, especially affecting the upper body High ai rway pressure reduces

venous return, again contri buting to oedema

Respiratory muscle wasting

Prolonged venti lation may l ead to di suse atrophy of the respiratory muscles

See also:

CO2 monitori ng, p92; Blood gas analysis, p100; Central venous catheter—use, p114; Central venous

catheter—insertion, p116; Bacteri ology, p158; Acute chest infection (1), p288; Acute chest i nfection (2), p290; Acute

respi ratory di stress syndrome (1), p292; Acute respiratory distress syndrome (2), p294; Pneumothorax, p300

IPPV—weaning techniques

Patients may requi re all or part of their respi ratory support to be provided by a mechani cal venti lator Weani ng from

mechanical ventil ati on may fol low several patterns In patients venti lated for short peri ods (no more than a few days)

it is common to al low 20–30min breathing on a ‘T’ piece before removing the endotracheal tube For pati ents who

have received l onger term ventilation i t i s unl ikely that mechani cal support can be wi thdrawn suddenl y; several

methods are commonl y used to wean these pati ents from mechanical venti lation There i s no strong evi dence that any

techni que i s superior i n terms of weani ng success or rate of weani ng

Intermittent ‘T’ piece or continuous positive airway pressure (CPAP)

Spontaneous breathing i s al lowed for increasingly prolonged periods with a rest on mechanical ventilati on i n between

The use of a ‘T’ pi ece for l onger than 30mi n may lead to basal atel ectasi s since the endotracheal tube bypasses the

physiological PEEP effect of the larynx It i s therefore common to use 5cmH2O CPAP as spontaneous breathing periods

get longer In the early stages of weani ng, mechanical venti lation is often conti nued at night to encourage sleep,

avoid fatigue and rest respiratory muscles

Intermittent mandatory ventilation (IMV)

The set mandatory rate i s gradual ly reduced as the spontaneous rate i ncreases Spontaneous breaths are usual ly

pressure supported to overcome ci rcuit and ventilator valve resistance Wi th this techni que it i s i mportant that the

patient's required minute ventil ati on is provi ded by the combi nation of mandatory breaths and spontaneous breaths

without an excessi ve spontaneous rate The reduction i n mandatory rate shoul d be slow enough to maintai n adequate

minute venti lation It is also i mportant that the patient can synchroni se hi s own respiratory efforts wi th mandatory

ventil ator breaths; many cannot, particul arl y where there are frequent spontaneous breaths, some of whi ch may

‘stack’ with mandatory breaths causi ng hyperi nflation

Pressure support ventilation

Al l respiratory efforts are spontaneous but positi ve pressure is added to each breath, the l evel being chosen to

mai ntain an appropri ate ti dal vol ume Weaning is performed by a gradual reduction of the pressure support l evel

whi le the respi ratory rate is <30/mi n The patient is extubated or al lowed to breathe wi th 5cmH2O CPAP when

pressure support is minimal (<10–15cmH2O wi th modern venti lators)

Choice of ventilator

Modern venti lators have enhancements to ai d weani ng; however, weaning most patients from ventil ati on is possi ble

with a basic venti lator and the i ntermittent ‘T’ piece technique, provi ded an adequate fresh gas fl ow is provided If

IMV and/or pressure support are used the ventil ator should provide the features l isted opposite

Key features in the choice of ventilator

Ventil ator must al low patient triggeri ng (i.e not a minute vol ume di vider)Fresh gas flow must be greater than spontaneous peak inspiratory fl ow

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IPPV—modes of venti lation, p8; IPPV—adjusti ng the venti lator, p10; IPPV—assessment of weaning, p18; Conti nuous

positive ai rway pressure, p26; Non-invasive respi ratory support, p32

IPPV—assessment of weaning

Assessment prior to weaning

Pri or to weaning i t i s important that the cause of respi ratory failure and any compl icati ons arising have been

corrected Sepsis shoul d be eradicated as shoul d other factors that increase oxygen demand Attention is requi red to

nutri tional status and fluid and el ectrol yte balance The diaphragm should be al lowed to contract unhindered by

choosi ng the optimum positi on for breathi ng (si tti ng up unl ess the diaphragm is paral ysed) and ensuri ng that

intra-abdomi nal pressure i s not high Adequate analgesia must be provided Sedatives are often withdrawn by thi s

poi nt but may stil l be needed in specific si tuations, e.g residual agi tation, rai sed intracrani al pressure Weani ng

should start after adequate explanation has been gi ven to the patient Factors predi cti ng weaning success are

detail ed in li st opposi te Spontaneous (pressure-supported) breathing should generall y start as soon as possi ble to

all ow reduction i n sedation l evel s, and maintai n respiratory muscle functi on Weani ng with the intention of removing

mechanical support i s unli kel y to be successful while FIO2 >0.4

Assessment during weaning

Continuous pulse oximetry and regular cli nical review are essenti al during weani ng Arterial blood gases should be

taken after 20–30min of spontaneous breathi ng After short term venti lation, extubate i f arterial gases and

respi ratory pattern remain satisfactory, the cough reflex i s adequate and the patient can cl ear sputum Pati ents bei ng

weaned from l onger term ventil ati on (>1 week) should generall y be al lowed to breathe spontaneously with CPAP for

at least 24h before extubation

Indications for re-ventilation

If spontaneous respiration is di scoordinate or the patient is exhausted, agitated or clammy, the ventilator shoul d be

reconnected However, cl ini cal moni toring shoul d avoi d exhaustion Successful weani ng is more easi ly accomplished i f

excessive fatigue is not al lowed to set in Tachypnoea (>30/mi n), tachycardi a (>110/mi n), respi ratory acidosi s (pH

<7.2), ri sing PaCO2 and hypoxaemi a (SaO2 <90%) shoul d all prompt reconnecti on of the ventil ator

Factors associated with weaning failure

Fai lure to wean is associated with:

Increased oxygen cost of breathingMuscle fatigue (hypophosphataemia, hypomagnesaemia, hypokalaemi a, mal nutri tion, peripheral neuropathy,myopathy and drugs, e.g muscle relaxants, ami noglycosi des)

Inadequate respi ratory drive (alkalosis, opiates, sedatives, malnutri ti on, cerebrovascular acci dent, coma)Inadequate cardi ac reserve and heart fai lure

In the latter case cardiac function shoul d be moni tored during spontaneous breathing peri ods Any deteri orati on in

cardi ac functi on should be treated aggressively (e.g optimal fluid therapy, vasodi lators, i notropes)

Factors predicting weaning success

PaO2 >11kPa on FIO2=0.4 (PaO2/FIO2 ratio >27.5kPa)

Minute vol ume <12l/minVital capaci ty >10ml/kgMaxi mum inspi ratory force (PImax) >20cmH2ORespiratory rate/tidal volume <100

Qs/Qt <15%

Dead space/ti dal volume <60%

Haemodynamic stabil ity

A ratio of respiratory rate to tidal volume (f/VT, shal low breathing i ndex) ≤v105 has been shown to have a 78%

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P.21

positive predi cti ve val ue for successful weaning

Key trial

Yang KL, Tobin MJ A prospecti ve study of i ndexes predi cting the outcome of tri al s of weani ng from mechani cal

ventil ation N Engl J Med 1991; 324:1445–50

See also:

IPPV—weaning techniques, p16; CO2 monitoring, p92; Blood gas anal ysi s, p100; Electrolytes

, p146; Calcium, magnesi um and phosphate, p148; Heart fail ure—assessment, p324; Acute weakness, p368; ICU

neuromuscul ar disorders, p388

High frequency ventilation

High frequency jet ventilation (HFJV)

A high pressure jet of gas entrai ns further fresh gas whi ch is di rected by the jet towards the l ungs Respi ratory rates

of 100–300/mi n ensure mi nute volumes of about 20l /mi n although tidal volume may be lower than dead space CO2

eli mi nation is usual ly more effi cient than conventional IPPV The method of gas exchange i s not ful ly elucidated but

includes turbulent gas mixing and convection Oxygenation i s dependent on mean ai rway pressure Peak ai rway

pressures are lower than wi th conventional mechanical venti lation but auto-PEEP and mean ai rway pressures are

mai ntained SaO2 often fall s when starting on HFJV, though usually improves wi th time The hi gh gas fl ow rates

employed require addi ti onal humi dification to be provided (30–100 ml/h); this is usuall y nebuli sed wi th the jet

Indications

Bronchopleural fi stula is the only proven ICU i ndi cation for HFJV though i t has been used to assist weani ng from

mechanical ventil ati on as the open circui t allows spontaneous breaths without the drawbacks of demand val ves HFJV

also ensures adequate venti lation if the pati ent fails to breathe adequatel y Reduci ng the drivi ng pressure and

increasi ng the respi ratory rate may facil itate weaning further In ARDS conventi onal ventil ati on can lead to ventil ator

trauma if a high VT i s used HFJV avoids problems associated wi th high VT but is often unable to provide adequate

ventil ation in isolation for patients with severe ARDS

Setting up HFJV

A jet must be provided via a modified endotracheal tube or catheter mount Entrai nment gas is provi ded vi a a ‘T’

piece The tidal volume cannot be set directl y Rather it is set by adjusti ng jet si ze, I:E rati o, drivi ng pressure and

respi ratory rate from an i n-buil t algorithm The respiratory rate i s usually set between 100–200/min As respiratory

rate i ncreases at a constant dri ving pressure the PaCO2 may i ncrease as i ncreasing PEEPi i ncreases the effective

physiological dead space The I:E ratio is usual ly set between 1:3 and 1:2 VT is determi ned by airway pressure and

I:E ratio Dri ving pressure i s usuall y set between 1–2bar These pressures are much hi gher than the 60–100cmH2O

used i n conventional ventil ation PEEPi i s related to the driving pressure, I:E ratio and respi ratory rate External PEEP

may be added to increase mean airway pressure should this be necessary to improve oxygenati on

Combined HFJV and conventional CMV

May be useful i n ARDS where HFJV alone cannot provide adequate gas exchange Low frequency pressure l imi ted

ventil ation wi th PEEP provi des an adequate mean airway pressure to ensure oxygenation whi le CO2 clearance is

effected by HFJV Care must be taken to avoi d excessi ve peak ai rway pressure when HFJV and CMV breaths stack

High frequency oscillation (HFO)

Thi s techni que can be appli ed externall y (see ‘Non-invasi ve respiratory support’) or via the endotracheal tube In the

latter i nstance high rates are appl ied and the dri ving pressure gradually increased The FRC increases, recruiti ng

alveol i and improving oxygenation The airway pressure can then be wound down, often without any signifi cant

deteri orati on in oxygenati on

Adjusting HFJV according to blood gases

Increasing PaO2

Increase FIO2

Increase I:E rati o

Increase drivi ng pressure

Add external PEEP

Consider reduci ng respi ratory rate

Decreasing PaCO2

Increase drivi ng pressure

Decrease respi ratory rate

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P.23P.24

See also:

Venti latory support—indicati ons, p4; Positive end expi ratory pressure (1), p22; Positive end expi ratory pressure (2),

p24; Acute respiratory distress syndrome (1), p292; Acute respi ratory di stress syndrome (2), p294

Positive end expiratory pressure (1)

Positi ve end expiratory pressure (PEEP) is a modali ty used i n posi tive pressure ventil ati on to prevent the alveoli

returning to atmospheri c pressure during expirati on It is routinely set between 3–5cmH2O; however, i n severe

respi ratory failure it wil l often need to exceed 10cmH2O to be above the l ower infl exi on point of the pressure–vol ume

curve This has been suggested as benefi ci al in patients with severe ARDS It rarel y needs to exceed 20cmH2O to

avoid cardiorespi ratory compl icati ons and al veolar over-distensi on (see below) It does not prevent nor attenuate

ARDS, or reduce capi llary leak or l ung water

Respiratory effects

PEEP i mproves oxygenation by recruiting coll apsed alveoli , redistri buting lung water, decreasi ng A–V mi smatch and

increasi ng FRC

Haemodynamics

PEEP usually lowers both left and ri ght ventricular prel oad and i ncreases RV afterl oad Though PEEP may i ncrease

cardi ac output in left heart fai lure and fluid overload states by preload reduction, i n most other cases cardi ac output

fal ls, even at rel ati vel y l ow PEEP l evel s PEEP may also compromise a poorly functioning ri ght ventricle Improved

PaO2 resulting from decreased venous admixture may someti mes ari se solel y from reductions in cardi ac output

Physiological PEEP

A smal l degree of PEEP (2–3cmH2O) is usuall y provided physiol ogi cally by a closed larynx It is lost when the pati ent

is intubated or tracheostomised and breathing spontaneously on a ‘T’ pi ece with no CPAP val ve (see CPAP)

Intrinsic PEEP (auto-PEEP, air trapping, PEEPi)

Increased l evel of PEEP due to insufficient time for expi ration, l eading to ‘air trapping’, CO2 retenti on, increased

airway pressures and increased FRC Seen i n pathological conditions of i ncreased airfl ow resistance (e.g asthma,

emphysema) and when insufficient expi ratory ti me is set on the ventilator Used cl inicall y i n i nverse ratio venti lation

to increase oxygenati on and decrease peak airway pressures High l evel s of PEEPi can, however, sl ow weaning by an

increased work of breathing; use of extrinsic PEEP may overcome thi s PEEPi can be measured by temporari ly

occluding the expi ratory outl et of ventil ator at end-expi ration for a few seconds to al low equil ibrati on of pressure

between upper and l ower airway and then reading the ventil ator pressure gauge (or pri nt-out)

‘Best’ PEEP

Ini ti all y descri bed as the level of PEEP producing the l owest shunt val ue Now generall y considered to be the l owest

level of PEEP that achieves SaO2≥90% all owi ng, wherever possi ble, l owering of FIO2 (i deal ly ≤0.6) though not at the

expense of peak airway pressures >35–40cmH2O or significant reductions in DO2

See also:

IPPV—descri pti on of ventil ators, p6; IPPV—modes of venti lation, p8; IPPV—adjusti ng the venti lator, p10;

IPPV—compli cations of venti lation, p14; Positive end expiratory pressure (2), p24; Conti nuous positi ve airway

pressure, p26; Lung recrui tment, p28

Positive end expiratory pressure (2)

A number of cli ni cal trial s have adjusted PEEP l evels according to FIO2 requirements (see tabl e) Al though unlikely to

consti tute ‘optimal PEEP’ for an individual patient, thi s provides a useful approxi mation and starti ng poi nt for further

ti tration of therapy

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Improvement of cardiac output i n l eft heart failureReduced work of breathi ng during weani ng in patients wi th high PEEPiNeurogeni c pulmonary oedema (i.e non-cardi ogenic pulmonary oedema foll owi ng rel ief of upper ai rwayobstructi on)

Complications

Reduced cardi ac output May need addi tional fl uid loadi ng or even i notropes This should generall y be avoi dedunl ess hi gher PEEP is necessary to maintai n adequate arterial oxygenation Caution shoul d be exercised inpati ents with myocardial ischaemi a

Increased ai rway pressure (and potential risk of venti lator trauma)

Overinflation l eading to ai r trappi ng and rai sed PaCO2 Use wi th caution i n pati ents with chronic ai rfl owlimitation or asthma In pressure- control led venti lation overdistensi on i s suggested when an i ncrease i n PEEPproduces a si gnifi cant fall in ti dal volume

High l evel s wil l decrease venous return, raise i ntracranial pressure and i ncrease hepati c congestion

PEEP may change the area of l ung in which a pul monary artery catheter tip is positioned from West Zone III tonon-Zone III This is suggested by a ri se in wedge pressure of at l east half the i ncrease i n PEEP and requiresresiti ng of the PA catheter

See also:

IPPV—descri pti on of ventil ators, p6; IPPV—modes of venti lation, p8; IPPV—adjusti ng the venti lator, p10;

IPPV—compli cations of venti lation, p14; Positive end expiratory pressure (1), p22; Conti nuous positi ve airway

pressure, p26; Lung recrui tment, p28; Pressure–volume rel ati onship, p96; Bl ood gas analysis, p100; Inotropes, p196;

Fluid chall enge, p274; Atel ectasis and pulmonary coll apse, p284; Rai sed i ntracrani al pressure, p382

Continuous positive airway pressure

Continuous posi ti ve airway pressure (CPAP) is the addi tion of posi tive pressure to the expiratory side of the breathi ng

ci rcuit of a spontaneously venti lating patient who may or may not be i ntubated This sets the basel ine upper ai rway

pressure above atmospheric pressure, prevents al veolar coll apse and possibly recrui ts al ready col lapsed al veoli It is

usuall y admi ni stered in increments of 2.5cmH2O to a maxi mum of 10cmH2O and appli ed via ei ther a ti ght-fi tting face

mask (face CPAP), nasal mask (nasal CPAP) or expiratory l imb of a ‘T’ pi ece breathi ng circui t A high flow (i.e above

peak i nspiratory flow) i nspired air-oxygen suppl y, or a l arge reservoir bag in the i nspiratory circuit, is necessary to

keep the val ve open CPAP improves oxygenati on and may reduce the work of breathi ng by reduci ng the

alveol ar-to-mouth pressure gradient in patients wi th high l evels of i ntrinsi c PEEP Transient periods of high CPAP

(e.g 40cm H2O for 40s) may be a useful manoeuvre for recruiting coll apsed alveoli and i mprovi ng oxygenati on in

ARDS

Indications

Hypoxaemia requi ri ng high respiratory rate, effort and FIO2.Left heart fail ure to improve hypoxaemia and cardiac output

Weaning modal ity

Reducing work of breathing i n pati ents with hi gh PEEPi (e.g asthma, chronic ai rfl ow limitati on) NB: use withcaution and moni tor closely

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P.29

P.30

Complications

With mask CPAP there i s an i ncreased ri sk of aspi ration as gastric di latation may occur from swallowed ai r

Insert nasogastric tube, especial ly if consciousness is impai red or gastric motil ity is reduced

Reduced cardi ac output due to reduced venous return (raised i ntra-thoraci c pressure) May need additional fluid

or even inotropes

Overinflation l eading to ai r trappi ng and hi gh PaCO2 Cauti on is urged in patients wi th chroni c airflow l imi tation

or asthma

High l evel s wil l reduce venous return and increase intracranial pressure

Occasi onal poor patient compli ance with ti ght-fi tting face mask due to feel ings of claustrophobi a and discomfort

on bri dge of nose

Inspissated secretions due to high flow, dry gas

Positi ve end expiratory pressure (1), p22; Positive end expiratory pressure (2), p24; Inotropes, p196; Fluid

chall enge, p274; Dyspnoea, p278; Airway obstruction, p280; Respi ratory failure, p282; Atelectasis and pulmonary

col lapse, p284; Acute chest infection (1), p288; Acute chest infection (2), p290; Acute respiratory distress syndrome

(1), p292; Acute respiratory distress syndrome (2), p294; Post-operati ve intensive care, p534

Lung recruitment

There has been considerable interest i n recent years in the concept of l ung recruitment The rational e i s that

reopening of collapsed alveoli wi ll resul t i n i mproved gas exchange, with resulting reducti ons in ai rway pressures and

FIO2 Timing i s crucial as coll apsed alveoli are more li kel y to be recrui table in the early stages of respiratory fail ure

It appears that benefit is more l ikely in non-respi ratory causes of ARDS, rather than in cases of direct pulmonary

pathol ogy such as pneumonia Some ani mal studies suggest that recrui tment procedures may even be potentially

injurious i n the latter si tuati on

Considerati on should be given to lung recrui tment soon after i ntuba-tion i n pati ents with severe respiratory fail ure,

and procedures causi ng de-recrui tment, e.g endotracheal sucti on and ai rway di sconnection

Recruitment techniques

A number of techni ques are descri bed to recruit collapsed alveoli , such as applying 40cmH2O PEEP for 40s wi th no

ventil ator breaths; del ivering a few large-volume, ventil ator-deli vered breaths; or by usi ng a combination of varyi ng

levels of PEEP and increasi ng pressure-del ivered breaths to obtain opti mal gas exchange

Al though anecdotal successes are reported, with occasionall y dramati c i mprovements in lung compli ance and gas

exchange, no comparati ve trial s have been performed, and outcomes have not been assessed prospecti vel y

Haemodynamic compromi se may occur during the procedure, though thi s usually recovers on cessati on

Key trial

Brower RG, et al for the ARDS Clinical Tri als Network Effects of recrui tment maneuvers in patients wi th acute

l ung i njury and acute respi ratory di stress syndrome venti lated with high posi tive end-expi ratory pressure Cri tCare Med 2003; 31:2592–7

Prone positioning

Prone positi oni ng is used to treat patients with acute respiratory distress syndrome (ARDS) to improve gas exchange

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