OXFORD DESK
`REFERENCE
`
`Carl Waldmann
`
`Andrew Rhodes
`
`PRAXAIR 1031
`
`i
`
`

`

`Oxford Desk Reference
`Critical Care
`
`Carl Waldmann
`Consultant in Anaesthesia and lrtens ve Care
`Royal Berkshire Hospital
`Reading
`
`Neil Soni
`Honorary Clinical Senio* Lecturer
`Division of Surgery, Oncclogy,
`Reproductive Biology and Anaesthetics
`Imperial College
`Landon
`
`and
`
`Andrew Rhodes
`Consultant in intensive Care
`St George's Hospital
`London
`
`OXFORD
`UNIVER SITY PRESS
`
`ii
`
`

`

`OXFORD
`UNIVERSITY PRESS
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`
`Oxygen therapy
`
`
`
`Aerobic respiration is the most efficient method of energy
`production ir the mammalian cell. it utilizes oxygen to
`produce adenosine triphosphate (ATP) The absence of
`oxygen or low oxygen levels result in more inefficient
`anaerobic respiration. Cellular energy levels become inad-
`ecuate, and this can lead to loss of cellular homeostasis,
`which in turn can lead to cellular death and very possibly
`organism death.A substantial part of critical care is targeted
`at treating and/or preventing hypoxia.
`
`
`
`Fathophysiology of oxygen delivery
`in critical illness the delivery (D01) and uptake (V01) of
`oxygen are often abnormal. Currently there are few thera-
`peutic strategies for improvement of VO;. Most methods
`of oxygen therapy target improvement in DOg.
`Delivery of oxygen from the environment is necessary to
`provide for cellular metabolism. ln single-celled organisms
`(e.g. amoeba). simple diffusion suffices. However, in the
`molt:-cellular, multi-organ human, more sophisticated
`illness.
`mechanisms have evolved, each with their problems in
`
`Clinical signs such as heart rate. blood pressure and L.-rire
`output can be misleading, especially in the young. This
`therefore requires the concept of an effective cardiac out-
`put (ECO). This couples the clinical signs with evidence of
`normal DO; and VO3 balance. The assessment includes
`peripheral temperature, oxygen haemoglobin saturation
`and arterial partial pressure. the presence of acidosis With
`a base excess greater than -2. lactataemia and abnormal
`SVO2 or ScvO;.Tht-.-se more techn,cal measures cfadequacy
`of oxygen delivery and uptake must always be taken in the
`clinical context, For example, in cyanide posoning. both
`circulatory and ventilatory indices appear normal, yet the
`severe acidosis and lactataemxa seen in this condition dem-
`onstratcs tissue hypoxia. Manipulating D03 by increasing
`the environmental oxygen fraction (F101) or cardiac output
`in this setting is unlikely to be helpful. and, even in sepsis and
`other more common types ofshock. achieving supranorrnal
`values for D01 is not thought to be beneficial
`Strategies for increasing DO;
`By assessing the type of hypoxia and its likely cause, the
`correct choice of DO;-improving strategy can be chosen.
`ln the critically ill, the commonly seen combination of
`mechanisms leading to hypoxia may require several tech-
`niques to be instigated in parallel. The methods for Improv-
`ing oxygen delivery to the tissues are based on reversing
`problems seen at each of the six stages of oxygen delivery.
`Improving the transport of oxygen once in the body Will be
`covered later in this book. This chapter is concerned with
`improving oxygen delivery from the environment to the
`bloodstream. Oxygen delivery at this stage should be
`considered a support mechanism, and treatment of the
`underlying cause is most important to reverse hypoxia,
`Oxygen therapy apparatus
`Principles
`
`in the hypoxic self-ventilating patient, delivery of oxygen to
`the alvenli
`is usually achieved by increasing the H07,
`Commonly this involves the application of one of the many
`varieties of oxygen masks to the face, such that it covers
`the mouth and/or nose. Each type of delivery system (‘on-
`slsts of broadly the same six components:
`1 Oxygen supply Delivery of oxygen can be from pres-
`surized cylinders, hospital supply from cylirder banks or
`
`Examples
`
`1. Low environmental oxygen (e.g altitude)
`2. Ventilatury failure (respiratory arrest. drug Overdose,
`ncuromuscular disease}
`1. Pulmonary shunt
`a. Ana‘omical—ventricular septal defect wizh right to left flow
`oedema. asthma
`I1.
`.Dl'ly5lDlDg»F3l~*Pl'lELl‘llDl'l3. pneummhorax, pulmonary
`Massive haemorrhage. severe anaemia, carbon monoxide
`poisoning. metnaemoglobinaemia
`Left ventricular failure. pulrronary embolism, hypovoiaemia
`hypothermia
`Cyan:de poisoning. arsenic poisoning, alcohol intoxication
`
`H
`
`Transport of oxygen to the cells follows six stages reliant
`only on the laws olphysics.
`1 Convection from the environment (ventilation),
`2 Diffusion into the blood.
`1 Reversible chemical bonding with haemoglobin.
`4 Convective transport to the tissues (cardiac output).
`5 Diffusion into the cells and organelles.
`6 The redox state of the cell.
`
`This chain of events is DO; Failure of D0; to match VO1
`leads to shock. This occurs when DO; declines to below
`approximately 300ml/min. Shock is defined loosely as fail-
`ure of delivery of oxygen to match tissue demand.
`Commonly this refers to circtlatory failure, but low D07,
`can result from several pathological mechanisms which can
`occur as a single problem or in combination (Table 1.1.1).
`The impact of low DO; can be made worse by an increase
`in VO1. Metabolic rate increases with exercise, inflamma-
`tion, sepsis, pyrexia. thryotoxicosis, shivering. seizures,
`agitation, anxiety and pain,This mismatch leads to the need
`for ea'ly detection of shock and prompt treatment, This
`has been shown to be beneficial in surviving sepsis.
`
`Table 1.1.1 Types 0‘ hypoxia
`
`T,',;. or hypoxia
`Hypoxir hypoxia
`
`Pathophysialogy
`Reduced supply of oxygen to the body leading
`to a low ar‘.E'ial oxygen tension
`
`Anaemic hypoxia
`
`Stagnant hypoxi
`Histotoxic”-hypoxia
`
`
`
`
`
`Normal "arterial oxygen tension’, but circulating’
`aerrogiohin is reduced orfunrtionally imoaired
`ClI’CL~lE.'.lOr1.
`allure oi oxygen transport due to inadequate
`
`Impaired cellulai metabolism of oxygen uespite
`adequate delivery
`
`002
`
`002
`
`

`

`zol
`
`ol
`O
`
`.c
`.
`30
`35
`25
`20
`1;
`10
`1
`Respiratory Rate (breath.min‘l)
`Fig. 1.1.1 The performance ofa Hudson non-rebreather mask on
`a model of human ventilation. Tidal volume of 500ml and four
`oxygen flow rates (ll/min (lJ),6l/min (<>).10l/min (A) and
`i5|/min (Oi). As the respiratory rate increases, so the effective
`inspired oxygen concentration (EIOC) deteriorates.
`
`Classification of oxygen delivery devices
`Methods of delivering oxygen to the conscious patient
`with no airway instrumentation can be broadly divided into
`the following categories.
`I Variable performance systems
`0 Fixed performance systems
`- High flow systems
`o Others
`
`Variable performance systems are so called because their
`FiOZ can vary as described above. Fixed performance sys-
`tems cannot. High flow systems use high oxygen flows to
`maintain a fixed performance. The common types and
`their properties are summarized in Table 1.1.3,
`
`Hazards of oxygen therapy
`Oxygen is a drug and. like most drugs. its use is not without
`risk. It
`is also a gas and commonly delivered from com-
`pressed sources.
`Supply
`Medical oxygen is supplied at 137bar from a cylinder. and
`4bar from hospital pipelines. Direct administration at deliv-
`ery pressures is highly dangerous and requires properly
`functioning pressure-limiting valves. Oxygen supports
`combustion. Patients must not smoke cigarettes when
`receiving oxygen therapy, and oxygen should be removed
`from the environment when sparking may occur, e.g. during
`defibrillation.
`
`a vacuum~insulated evaporator (VlE), or an oxygen con-
`centrator.
`
`Oxygen flow control. For example an OHE ball valve
`flow meter.
`i
`
`Connecting tubing. Both from supply to control, and
`from control to patient.The bore of the tubing is impor-
`tant as it has effects on the oxygen flow rate. lnrsome
`systems it car also act as a reservoir:
`Reservoir. All have reservoirs. in the simple ‘oxygen
`mask it
`is
`the mask itself. Nasal cannulae use the
`nasopharynx as the reservoir. An oxygen tent is a large-
`volume reservoir. The reservoir serves to store oxygen,
`but must not allow significant storage of exhaled gases
`leading to rebreathing of carbon dioxide.
`Patient attachment. This permits delivery of oxygen to
`the airway. This is achieved either by directly covering
`the upper airway, e.g. plastic mask/head box. or by
`increasing the oxygen concentration in the wider envi~
`ronment, e.g. oxygen tent.
`Expired gas facility. Expired gas needs to dissipate to the
`environment This can be achieved by having a small reser-
`voir with holes, one-way valves as in the non-rebreather
`masks, or high oxygen flows as seen in some of the con-
`tinuous positive airway pressure (CPAP) systems.
`Additional features of oxygen breathing systems are the
`presence of humidification such as a water bath. to prevent
`drying of the mucosal membranes. Some devices have an
`oxygen monitor incorporated into the apparatus to permit
`more accurate defining of the H02.
`Factors that affect the performance ofoxygen
`delivery systems
`Most of the simpler oxygen delivery devices, e.g. plastic
`masks, nasal cannulae, etc.. deliver oxygen at relatively low
`oxygen flow rates. The patient inspiratory flow rate varies
`throughout inspiration (25elO0+L.min“') and exceeds the
`oxygen flow rate,This drains the small reservoir and causes
`entrainment of environmental air. The effect is to dilute the
`oxygen concentration to the final FiO;_. The actual HO;
`that reaches the alveolus is therefore unpredictable and is
`dependent on the interaction of patent factors and device
`factors (Table 1.1.2). In the hypoxic patient it is common to
`‘End significant increases in inspiratory flow rates as well as
`he loss of the respiratory pause. This causes significant
`entrainment of air, lowering the alveolar FiO1. This is par-
`ticularly true ofthe variable performance masks. but is also
`seen in Venturi-type masks, particularly when higher HO]
`inserts are used.The presence of a valve-controlled reser-
`voir oag on a non-rebreather mask should compensate for
`high inspiratory flows, hence the belief that such devices
`can deliver an HO; of 1.0 which does not actually happen.
`This is not seen in models of human ventilation (Fig. 1.1.1)
`
`Table 1.1.7. Factors that influence the HO; delivered to a
`patient by oxygen delivery devices5
`Patient factors
`
`Device factors
`
`Oxygen flow rate
`ice,-ratory flow rate
`ce ofa respiratoryV W V Volume ofrnask H ‘
`Air vent size
`Tightness of fit
`
`i i
`
`s
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`003
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`

`;z=vwAisstArrf
`
`I
`
`Table 1.1.3 Classification of oxygen delivery systems
`Oxygen delivery Types used
`system
`
`Properties
`
`Variable
`pcrtoriiiancc
`
`Fixed
`performance
`
`Higiiri
`systems
`
`Other;
`
`Nasal carnulae. semi~rigid masks
`(Hudson MC), no-i-resreathing masks,
`tracheostomv mask. T
`ce systems
`Venturi—type masks, a
`. etic
`breathing circuits (waters circuit.
`AmDl1'bag)
`
`” "rli5i;c'c‘§y§¢n§s.v5,;};iHé}iri®
`(hurndified higli flow nasal cannciae)
`
`Non sealed masks or nasal cannulac. Oxygen at .ow flow ().—1bI.n-in“).
`Small ‘eservolr. Significant entrainment of envirmmental air. Accurate HO:
`not possible. Comfortable 3'ld simple to use
`Venturi-typo masks rely on the Venturi principle to dilute oxygen
`predictably to FSO2. Need to change valve to alter HO; Higher HO; valves
`have larger oriiices, so behave more like a variable performance system.
`Comfort bl
`. Simple to use, bur needs attention to detail
`Anaesthetic breathing systems require sealing l'|'l3S\' to prevent entrainment.
`Valves prevent rebreathirig. Large reservoir: Accurate HO). Scaled mask can
`be uncomfortable. Knowiedge of breathing systems required.
`Rely on hilghvoxlygen flows to match patient’: inspiratory flow rate. Small
`reservoirs and sealed mask or nasa-pharynx. Requires humidification.
`Accurate H02. Scaled mask uncomfortable with risk of mucosal dryness.
`More complicated to set up.
`intravascular oxygenation
`Unusual i'i the seiflventilat nglpatientitlxygenatioii achieved across
`7
`I P
`‘Q
`l’
`_
`cardiupulmonzir bv ass. interventional
`s nthetic mernoranc. CO; removal can be an issue. FiO2 can ne difficult to
`lung assist devizes (Novolungfi, ECMO) measure. Complicated and limited to specialist centres
`
`H
`
`Oxygen toxicity
`CNS toxicity {Paul Bert effect)
`Seen in diving, oxygen delivered at high pressures (>3atm)
`seizures.
`can lead to acute central nervous system (CNS) signs and
`
`Lung toxicity (Lorraine Smith effect)
`Prolonged exposure to a high HO; results in pulmonary
`injury. Possibly mediated by free oxygen radicals. there is a
`progressive reductior in lung compliance, associated with
`interstitial oedema and fibrosis. Avoidance of long periods
`of high oxygen concentrations reduces this effect. Clinically
`it can be difficult to prevent long exposure times; however,
`in general, patients should remain below an FiO1 of 0.5
`where possible and not remain above this value for much
`longecthan 30h.
`Bronchopulmonary dysplasia (BPD)
`A condition concerning neonates, it is a chronic fibrotic
`lung disease associated with ventilation at high FiO2.
`Pathologically it is similar to the adult condition above, but
`with the additional effect of immaturity. Surfactant and
`maternal steroid therapies have lowered the incidence and
`severity.
`Retinopathy ufprernaturlty
`This is a vasoproliferative disorder ofthe eye affecting pre-
`mature neonates. lnitially thought to be solely due to the
`use of high FiO;, its continued incidence despite tighter
`oxygen control suggests that other factors associated with
`prematurity are involved.
`
`Hyperbaric oxygen therapy
`Oxygen can be delivered to patients at higher than atmos-
`pheric pressures (2~3atm). This serves to increase the
`amount of oxygen dissolved in the plasma, rather than that
`bound to haemoglobin.At rest, the metabolic demands of
`an average person can be met by dissolved oxygen alone
`when breathing an F102 of 1.0 at 3atm.
`Hyperbaric oxygen is delivered in a sealed chamber. The
`gas is warmed and humidified.The common ind.cations for
`hyperbaric oxygen therapy are listed in Table 1.1.4. High
`
`Table 1.1.4 Suggested indications for hyperbaric oxygen
`therapy
`
`Prirriary therapy
`Carbon monoxide poisoning
`Air or gas embolism
`Decompression sickness
`(the ‘i>encs')
`
`Adjunctive therapy
`Radiation tissue damage
`Crush iniuries
`Acute blood loss
`
`.
`"‘Y°”°"°5l5
`
`Compromised skin flaps or grafts
`Refractory os:eomyelitis
`lntracranial abscess
`Enhancement of healing o‘
`prob:em wounds
`
`pressure therapy also has important side effects. Whilst
`clearly of value in these situations, the availability of a
`hyperbaric chamber often reduces its use, particularly in
`carbon monoxide poisoning.
`Further reading
`Dellinger RP, Carlet JM, Mascr H, et oi. Surviving Sepsis Campaign
`guidelines for management of seven: sepsis and septic shock. Crit
`Care Med 2004,’ 32: B5BV73.
`Gattinoni L, Brazzi l, Pelosi P. ez ai. A trial of goal-oriented hemo-
`dynamic therapy in critically ill patients. SvOl Collaborative
`Group N Engij Med 1995; 333: 1025 32.
`Grocott M. Montgomery H, Vercueil A. High-altitude physiology
`and pathophysiology: implications aric relevance for il‘[EF‘SlVC
`(arc medicine. Cm Core NW; 11:103.
`Hayes MA,Tim1iins AC,Yai. EH, et ai. Elevation ofsystemic oxygen
`delivery in the treatrrent of ciitically ill patients. N Englj Med
`1994;33Ci:171.7~22.
`leigh
`Variation in performance of oxygen therapy devices.
`Anaesthetic ‘I970; 25: 21042.
`Stoller KFl Hyperbaric oxygen and carbon monoxide poisoning: a
`critical rev ew. Neural Res 100719‘ 14645.
`Tibbles PM. Edels‘oergJS. l‘lYp€l'lJaFlC-OXygE|'I
`therapy. N Eng!) Med
`- 1996;334:1647. E.
`
`W'agstaflT/ll, Soni N. Per‘nr.'ri_arice of six types of oxygen delivery
`devices at varying respiratory rates. /lnaestresia 2007, 62,
`492-503.
`
`‘i5i
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`E2é2
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`

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`OXFORD DESK REFERENCE
`
`Critical care medicine is an evolving speciality in which the amount of available information is
`growing daily and spread across a myriad of bool<s,journals and websites.This essential guide brings
`together this information in an easy-to-use format. Up-to-date evidence—based information on the
`management of the critically ill is combined in one resource, ideal for the desktops of intensive Care
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`To facilitate the key aim of rapid and easy access to information,the book is designed so that each
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`With chapters written by internationally renowned critical care specialists and edited by three of
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`Oxford Handbook of Critical Care,Third Edition
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