`
`OXFORD DESK
`REFERENCE
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`Andrew Rhodes
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`Carl Waldmann Neil oni
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`“Oxford Desk Reference
`Critical Care
`
`Carl Waldmann
`Consultant in Anaesthesia and lr‘cens ve Care
`Royal Berkshire Hospital
`Reading
`
`Neil Soni
`Honorary Clinical Senio” Lecturer
`Division of Surgery, Oncology,
`Reproductive Biology and Anaesthetics
`Imperial College
`Lendon
`
`and
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`Andrew Rhodes
`Consultant in intensive Care
`St George's Hospital
`London
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`OXFORD
`UNIVER SITY PRESS
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`ii
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`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 inefficiert
`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 a‘id very possibly
`organism death.A substantial part of critical care is targeted
`at treating and/or preventing hypoxm.
`
`Clinical Signs such as heart rate. blood pressure and urire
`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 V03 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
`SvOz or chO;.These more technical measures ofadequacy
`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-
`onstrates tissue hypoxia. Manipulating D02 by increasing
`the environmental oxygen fraction (Flog) or cardiac output
`in this setting is unlikely to be helpful. and, even in sepsis and
`other more common types oishock. achieving supranormal
`values for D01 is not thought to be beneficial
`Stmtegies for increasing DO;
`By assessing the type of hypoxia and its likely cause, the
`correct choice of DOyimproving strategy can be chosen.
`in 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 selloventilating patient, delivery of Oxygen to
`the alveoli
`is usually achieved by increasing the HOT.
`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 ron-
`sists of broadly the same six components:
`1 Oxygen supply Delivery of oxygen can be from pres-
`surized cylinders, hospital supply from cylirder banks or
`
`
`
`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 V03. 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
`
`Transport of oxngn to the cells follows six stages reliant
`only on the laws ofphysics.
`1 Convection from the environment (ventilation),
`2 Diffusion into the blood.
`] 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 00;, Failure of D0; to match V01
`leads to shock. This occurs when D01 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 1.11).
`The impact of low D02 can be made worse by an increase
`in V01. Metabolic rate increases with exercsse, inflamma-
`tion, sepsis, pyrexia. thryotoxicosis, shivering. seizures,
`agitation, anxiety and painThis mismatch leads to the need
`for ea'ly detection of shock and prompt treatmentThis
`has been shown to be beneficial in surviving sep5isi
`
`Table 1.1.1 Types ol hypoxia
`
`Examples
`Pathophysiology
`was o( hypoxia
`
` Hypoxic hypoxia Reduced stpply of oxygen to the body leading
`1. Low environmental oxygen (eg altitude)
`to a low arte'ial oxygen tension
`2i Ventilatury failure (respiratory arresL drug overdose,
`neuromuscular discasci
`1. Pulmonary shunt
`a. Ana‘ornical—ventricular septal defect wizh right to left flow
`oedema. asthma
`I). Physiologicalwpneuinpriia. pneummhorax, pulmonary
`Massive haemorrhagci severe anaemia, carbon monoxide
`poisoning. metnaemoglobinaemia
`Left ventricular failure. puin-onary embolism, hypovoiaernia
`hypothermia
`Impaired cellular metabolism of oxygen despite
`Cyanide poisoning. arsenic poisoning, alcohol intoxication
`adequate delivery
`
`
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`Normal arterial oxygen tension, but circulating
`aerrogiohin is reduced orfu'irtionally imoaired
`
`circclazion,
`allure oi oxygen transport due to inadequate
`
`Stagnant hypoxi
`Histotoxic hypoxia
`
`Anaemic hypoxia
`
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`a vacuum~insulated evaporator (VlE), or an oxygen con»
`centrator.
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`10C-
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`2 Oxygen flow control. For example an OHE ball valve
`flow meter.
`‘
`
`3 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. lnflsome
`systems it car also act as a reservoir:
`‘
`4 Reservoir. All have reservoirs. in the simple ‘oxygen
`mask it
`is
`the mask itself. Nasal cannulae use the
`nasopharynx as the reservoinAn 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.
`5 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.
`5 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 FiOZ.
`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 (25400+L.min“‘) and exceeds the
`oxygen flow rateThis drains the small reservoir and causes
`entrainment of environmental air. The effect is to dilute the
`oxygen concentration to the final FiOz. The actual FiOz
`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
`find significant increases in inspiratory flow rates as well as
`the loss of the respiratory pause. This causes significant
`entrainment of air, lowering the alveolar FiOl. This is par-
`ticularly true ofthe variable performance masks. but is also
`seen in Venturi»type masks, particularly when higher HO]
`Inserts are usedThe 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 1.1.2 Factors that influence the no: delivered to a
`patient by oxygen delivery devicess
`Patient factors
`Device factors
`
`l5‘3,'ifl[3FY flow rate
`Ox en flow rate
`
`one of a respiratory pause
`I?
`Volume of mask
`
`».a. volume
`Air vent size
`
`
`Tight-ness‘of'fit
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`80-
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`60~ EiOCa.)
`
`40
`
`zol
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`ol
`.
`.-
`O
`20
`30
`3S
`
`S
`
`10
`
`15
`
`25
`
`I
`Respiratory Rate (breathmin‘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 (Ll),6l/min (O).10l/min (A) and
`iSI/min (0)). 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
`0 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, eg. during
`defibrillation.
`
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`awAps‘rArr:
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`Table 1.1.] Classification of oxygen delivery systems
`
`Oxygen delivery Types used
`Properties
`system
`
`Variable
`Nasal cannulae‘ semi~rigid masks
`Non sealed masks or nasal cannulac. Oxygen at .ow flow (l—ibln‘in“).
`tracheostomv mask. T
`pcrtorrriancc
`(Hudson MC), non-reareathing masks,
`Small ‘eservoir. Significant entrainment of environmental air. Accurate FiO:
`ce systems
`not possible. Comfortable and simple to cse
`
`Venturitype masks, a
`. ctic
`Venturi-typc masks rely on the Verituri principle to dilute oxygen
`breathing circuits (waters circuit.
`predictably to Flo). Need to change valve to alter FiO; Higher FiO; valves
`
`have larger orifices. so behave more like a variable performance system.
`Amou-bag)
`Comfort bl
`_ Simple to use, but needs attention to detail
`Anaesthetlc breathing systems require sealing masc to prevent entrainmem.
`Valves prevent rebreathlrig. Large resethiir. Accurate HO). Sealed mask can
`be uncomfortable Knowiedgc of breathing systems required.
`Rely on highvox‘ygen flows to match patients inspiratory flow rate. Small
`reservoirs and sealed mask or naso~pharynx Requires humidification.
`Accurate FiOZ. Scaled mas‘x uncomfortable with risk of mucosal dryness.
`More complicated to set up.
`intravascular oxygenation
`Unusual in the sellrveritilat rig patient. Oxygenation achieved across
`7
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`‘
`Y
`.
`cardiopulmonar bv ass. interventional
`s nthetic memoranc. C01 removal can be ari issue. FiO; can he difficult to
`lun assist devi:es (Novolun J, ECMO measure. Corn licated and limited to s Cialist canvas
`P
`P9
`3
`E l
`
`
`'rlbiéc'c' syétérns.vépéih'eiin®
`(hum-dified high flow nasal cannciae)
`
`
`
`Fixed
`pen‘ormance
`
` High A
`systems
`
`Others
`
`Table 1.1.4 Suggested indications for hyperbaric oxygen
`therapy
`
` Primary therapy Adjunctive therapy
`
`Carbon nonoxide poisoning
`Radiation tissue damage
`A”. 6:22.35. embolism . , ., Crush injuries”
`.,
`.
`D'e'céiriaééssibi} gains; "
`‘ Xfiuie'isibcid loss
`(the ‘oencs')
`
`.
`myonecrosis
`
`,,
`
`,
`
`Compromised skin flaps or grafts
`Refractory os:eomyelitis
`lntracranial abscess
`Enhancement of healing o‘
`probe”) 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
`Dellrnger RP, Carletlr’l, Mastr H, et ah Surviving Sepsis Campaign
`guidelines r'o' management of severe sepsis and septic shock. Crit
`Care Med 2004; 32: ESE-V73.
`Gatlinoni L, Brazzi l, Pelosi P. ez al. A trial of goal-oriented heme
`dynamic therapy in critically ill patients. SvOy Collaborative
`Group N Englj Med 1995; 333: 1025 32.
`Grocott M. Montgomery H. Vercueil A, High-altitude physiology
`and pathophysiology: implications anc relevance for irtensivc
`care medicine. Cm Care 1001111103.
`Hayes MATimninsACXai. EH, er al. Elevation oisystemic oxygen
`delivery in the treatrrent of critically ill patients. N Engl} Med
`1994;330:171742.
`leigh j Variation in performance of oxygen therapy devices.
`Anaesthesia 1970125121042.
`Stoller KFl Hyperba’ic oxygen and carbon monomoe poisoning: a
`critical rev ew. Neural Res 1007: 29‘ 14645.
`Tibbles PM. Edels'oergJS. Hyperbariooxygen therapy. N Engl) Med
`- 1996;334:1647. E.
`
`W'agstaflTA), Soni N. PEr‘nrmance of six types of oxygen delivery
`devices at varying respiratory rates. Anaesthesra 2007, 62,
`492—503.
`
`
`
`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 FiO; results in pulmonary
`injury. Possibly mediated by free oxygen radicals. there is a
`progressive reductior in lung compliance, associated with
`interstitial oedema and fibroos. 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 Fiol of 0.5
`where possible and not remain above this value for much
`longecthan 30h.
`Bronchoipulmonary dysplasia (BPD)
`A condition concerning neonates, it is a chronic T'ibrotic
`lung disease associated with ventilation at high FiOz.
`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 ofprernaturity
`This is a vasoproliferative disorder ofthe eye affecting pre-
`mature neonates. lnitially thought to be solely due to the
`use of high HO; 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 haemoglobinAt rest, the metabolic demands of
`an average person can be met by dissolved oxygen alone
`when breathing an F102 of 1.0 at 3am.
`Hyperbaric oxygen is delivered in a sealed chamber. The
`gas is warmed and humidifiedThe common ind.cations for
`hyperbaric oxygen therapy are listed in Table 1.1.4. High
`
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`OXFORD DESK REFERENCE
`fiftiglifigai Qfifig
`
`Critical care medicine is an evolving speciality in which the amount of available information is
`growing daily and spread across a myriad of books,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
`Units, High Dependency Units, acute medical or surgical wards, Accident & Emergency departments
`and operating theatres.
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`To facilitate the key aim of rapid and easy access to information,the book is designed so that each
`subject forms a self-contained topic in its own right, laid out across two or four pages.This makes
`the information included simple to find, read, and absorb. so that the book can be consulted in the
`clinic or ward setting for information on the optimum management ofa particular condition.
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`With chapters written by internationally renowned critical care specialists and edited by three of
`the leading figures in UK critical care, this book should never be far from the critical care physician's
`fingertips.
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`Oxford Handbook of Critical Care,Third Edition
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