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182 PART IV MANAGEMENT CONSIDERATIONS
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Fleisher LA, Fleischmann KE, Auerbach AD, et al.: 2014 ACC/AHA Guideline on perioperative cardiovascular evaluation and
management of patients undergoing noncardiac surgery: executive summary, Circulation, August 1, 2014. [published
online].
Glick M: New guidelines for prevention, detection, evaluation, and treatment of high blood pressure, J Am Dent Assoc
129:1588–1594, 1998.
Goldman L, Caldera DL, Nussbaum SR, et al.: Multifactorial index of cardiac risk in patients in noncardiac surgical proce-
dures, N Engl J Med 297:945–950, 1977.
McCabe JC, Roser SM: Evaluation and management of the cardiac patient for surgery, Oral Maxillofac Surg Clin North Am
10:429–443, 1998.
Muzyka BC, Glick M: The hypertensive dental patient, J Am Dent Assoc 128:1109–1120, 1997.
Seres T: Congestive heart failure. In Duke J, editor: Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.
Wilson W, Taubert KA, Gewitz M, et al.: Prevention of infective endocarditis: guidelines from the American Heart Association:
a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee,
Council on Cardiovascular.

PaO2= 100.1 − (0.323 × age in years)
RESPIRATORYDISORDERS
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Yedeh Ying, Zachary S. Peacock, Osama Soliman
1. What is the normal adult oxyhemoglobin dissociation curve for blood at 37%, pH
of 7.4, and PCO2 of 40 mm Hg?
See Fig. 17-1.
2. What are the general rules concerning the dissociation curve shifts?
• AlowpHorahighPCO2shiftsthecurvetotheright.
• AhighpHoralowPCO2shiftsthecurvetotheleft.
• Elevatedbodytemperatureshiftsthecurvetotheright.
• Lowerbodytemperatureshiftsthecurvetotheleft.
• Carbonmonoxideinthebloodincreasestheafnityofremainingoxygenforhemoglobinandshifts
thecurvetotheleft.
3. How does the interpretation of the curve change when the curve shifts to the left?
TheP50isaconventionalmeasureofthehemoglobinafnityforoxygen.Ifthecurveisshiftedto
theleft,thereislessPO2(mmHg)inthebloodneededtoachievetheP50.Inotherwords,thereisan
increasedhemoglobinafnitytoO2withaleftcurveshift.
4. What is 2,3-diphosphoglycerate (2,3-DPG)?
Itisproducedbyerythrocytesandnormallyispresentinfairlyhighconcentrationsinredbloodcells
(RBCs).
5. When is 2,3-DPG produced?
Itisproducedmainlyduringchronichypoxicconditions.Anincreasein2,3-DPGshiftsthecurvetothe
rightandallowsmoreO2tobereleasedfromhemoglobinataparticularO2level.Withadecreasein
2,3-DPG,thecurvewillshifttotheleft,indicatinganincreasedafnityforO2byhemoglobin.HemoglobindoesnotreleaseO2inthetissuesexceptataverylowPO2.
6. How does 2,3-DPG affect blood supply in blood banks?
Bloodstoredforaslittleas1weekwillhavedepleted2,3-DPGunlessstepsaretakentorestore
normallevelsof2,3-DPG.
7. How does the aging process affect PaCO2?
PaCO2andalveolarventilationareunchangedbytheagingprocess.
8. How does the aging process affect PaO2?
PaO2decreaseswithage.Thisdecreasecanbecalculatedaccordingtothefollowingformula:
CHAPTER 17
ThusthePaO2ofa30-year-oldpersonwouldbecalculatedas100.1−(0.323×30)=90.41.
9. What are the anatomic volumes of the lungs?
TV:tidalvolume,theamountofairmovedwitheachbreath(Fig. 17-2)
IRV:inspiratoryreservevolume,themaximumadditionalamountofairthatcanbeinhaledafterthe
endofinspiration
IC:inspiratorycapacity,themaximumvolumeofairthatcanbeinspired(VT+IRV)
RV:residualvolume,theremainingvolumeofairaftermaximalexpiration
ERV:expiratoryreservevolume,themaximumadditionalamountofairthatcanbeexhaledafter
expiration
FRC:functionalresidualcapacity,thevolumeinthelungsafterpassiveexpiration(RV+ERV)
VC:vitalcapacity,themaximumamountofairthatcanbeexhaledaftermaximuminspiration
(IC+ERV)
TLC:totallungcapacity,thevolumeinthelungsatmaximalinspiration(RV+VC)
183

184 PART IV MANAGEMENTCONSIDERATIONS
6000mL
Time
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Percent saturation
hemoglobin
Increased affinity
Acute alkalosis
100
Decreased PCO
Decreased temperature
Low levels of 2,3 DPG
90
Carboxyhemoglobin
Methemoglobin
80
Abnormal hemoglobin
70
60
50
40
30
20
10
0
2
Normal
Decreased affinity
Acute acidosis
High CO
2
Increased temperature
High levels of 2,3 DPG
Abnormal hemoglobin
200
Figure 17-1. Normaloxyhemoglobindissociationcurve.DPG,Diphosphoglycerate;COHb,carboxyhemoglobin;Hb,hemoglobin. (From Cairo JM, Pilbeam SP: Mosby’srespiratorycareequipment, ed 9, St Louis, 2009, Mosby.)
40 60
PO
(mm Hg)
2
80 100
Maximum
5000mL
4000mL
3000mL
2000mL
1000mL
inspiration
Maximum
expiration
Inspiratory
reserve
volume
Tidal volume
Expiratory
reserve
volume
Residual volume
Vital
capacity
Inspiratory
capacity
Functional
residual
capacity
Total
lung
capacity
0
Figure 17-2. Lungvolumesandcapacities. (From Nagelhout JJ, Plaus K: Nurseanesthesia, ed 4, St Louis, 2010,
Saunders.)

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10. What are pulmonary function tests (PFTs), and why are they used?
PFTsareanadjuncttohistoryandphysicalexaminationandprovideanoverallassessmentofthe
respiratorysystem.Thetestsinclude(1)measurementsofairow(spirometry),(2)lungvolumes,and
(3)diffusingcapacityforinspiredcarbonmonoxide(DLCO).Thetestsarereportedasapercentageof
predictednormalvaluesbasedonageandheight.
11. What useful measurements are used in spirometry?
FVC:Forcedvitalcapacity
FEV1:thevolumeofairthatcanforciblybeblownoutin1second,afterfullinspiration
FVC/FEV1ratio:knownastheTiffeneau-Pinellindex
12. What is the normal FVC/FEV1 ratio?
ThenormalFVC/FEV1ratiois70%to80%.
13. What is the FVC/FEV1 ratio in obstructive and restrictive disease?
Inobstructivepulmonarydisease,expiratoryresistanceincreases,resultinginanincreaseintheFEV1.
TheFVCmayalsoincrease,butnottothesameextent,resultinginadecreasedratiobelow70%.In
restrictivediseasesuchaspulmonarybrosis,theFVCandtheFEV1arebothreducedproportionally,
resultinginanormalratioorevenincreasedasaresultofdecreasedlungcompliance.
14. How is the forced expiratory volume in 1 second (FEV1) changed with age?
FEV1declineslinearlywithageincrease.
15. What are the most significant changes of pulmonary function associated with aging?
• Lossoflungelasticity,whichleadstoincreasedmeanalveolardiameterandvolumeandreducedFEV
• Decreasedpoweroftherespiratorymusculature
1
• Increasedrigidityofribcage
Allthesechangesstartbecomingapparentinthethirddecadeoflife.
16. What is the normal rate of breathing?
Thenormalrespiratoryrate(RR)is10to20breaths/mininadolescentsandadults(>12yearsold),
30to60ininfants(0to1year),24to40intoddlers(1to3years),22to34inthose3to6yearsold,
and18to30inthose6to12yearsold.Foradolescentsandadults,anRR>20/minisconsidered
tachypneaand<10/minisbradypnea.
17. Where is the respiratory center?
Therespiratorycenterisawidelydispersedgroupofneuronslocatedbilaterallyinthereticular
substanceofthemedullaoblongataandpons.
18. What influences the respiratory center?
ExcessCO2andhydrogenions(H+)affectrespirationmainlybydirectexcitatoryeffectsontherespi-
ratorycenteritself.Oxygendoesnothaveasignicantdirecteffectontherespiratorycenter.O2acts
almostentirelyperipherallyonthecarotidandaorticbodies.
19. What does PEEP mean?
PositiveEnd-ExpiratoryPressureduringmechanicalventilation.PEEPaidsinpreventingalveolarand
smallairwaycollapseandmayhelprecruitlungunitsthatwerepreviouslycollapsed.
20. What are the beneficial effects of PEEP?
• Increasedfunctionalresidualcapacity
• Increasedcompliance
• IncreasedPaO
• Increasedventilation–perfusion(V/Q)ratio(wheninitiallylow)
2
• Decreasedpulmonaryshunt
21. What is the effect of PEEP on cardiac output?
BecauseofincreasedintrathoracicpressureanddecreasedvenousreturnwhenusingPEEP,cardiac
outputmaybedecreased.
22. What are the normal blood gas values?
pH7.40±0.05units
(H+)40±5mEq/L

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PCO240±5mmHg
A0.1decreaseinpHcorrespondstoa12mmHgofPCO2increase,whichequalsabasechangeof6mEq/L.
• Goldenruleno.1:ApHof0.08=PaCO2of10mmHg.
• Goldenruleno.2:ApHof0.15=basechangeof10mEq/L.
23. What are the common causes of acid–base disorders?
• Respiratoryalkalosis:hyperventilation,sepsis,anxiety,pain
• Respiratoryacidosis:CNSdepression,neuromusculardisorders,upperandlowerairway
abnormalities
• Metabolicalkalosis:emesis,volumedepletion,nasogastrictube(NGT)drainage,diureticuse,
exogenousalkali,mineralocorticoidexcess
• Metabolicacidosis:ketoacidosis,lacticacidosis,renalfailure,ingestionoftoxins(e.g.,methanol
andpropyleneglycol)
24. How is the diagnosis of respiratory acidosis made?
Respiratoryacidosisisusuallyevidentfromtheclinicalexam,especiallyifrespirationisobviously
depressed.Analysesofarterialbloodgases(ABGs)willconrmthediagnosis.ArterialpHwillbe
<7.35,andPCO2willbe>45mmHg.
25. What are some causes of respiratory acidosis?
Anydiseaseorconditionthatmayaffecttherespiratoryfunctioncancauserespiratoryacidosis,
including:
• Chronicobstructivepulmonarydisease(COPD)
• Chestwallorairwayinjury
• Drugeffects
• Pulmonaryedema
• Centralnervoussystem(CNS)depression
• Cardiacarrest
• Extremeobesity(e.g.,pickwickiansyndrome)
• Pneumonia
26. How is the diagnosis of respiratory alkalosis made?
Clinically,respiratoryalkalosisusuallymanifestsashyperventilation.However,dependingonitssever-
ityandacuteness,hyperventilationmaynotbeevident,butananalysisofABGswilldemonstratean
arterialpHof>7.45andaPCO2of<35mmHg.
27. What are some causes of respiratory alkalosis?
• Hyperventilation
• Pulmonaryembolus
• CNSinjury
• Excessivemechanicalventilation
• Fever
28. What is Cheyne-Stokes breathing?
Periodsofhyperpnea(deepbreathing)alternatingwithperiodsofapnea.Thecrescendo–decrescendo
patternofbreathingisassociatedwithchangesinPO2andPCO2.Childrenandtheelderlynormally
showthispatterninsleep.Innormaladults,causesofthispatternofbreathingincludeheartfailure,
uremia,drug-inducedrespiratorydepression,andbraindamage.
29. What are the causes of hypoxemia?
• Lowinspiredoxygenconcentration(lowFiO2):wheninadequateoxygenlevelissuppliedoravail-
able(e.g.,asphyxiation)
• Hypoventilation:inadequateminuteventilation(e.g.,sedationorCNSdepression,brainstemstroke)
• Righttoleftshunt:perfusionwithoutventilation;whenbloodbypassesthepulmonarysystemby
owingfromtherighthearttotheleftwithoutexposuretoinhaledoxygen(e.g.,atrialorventricular
septaldefect,pulmonaryedema,pneumonia)
• Ventilation/perfusionmismatch:Ventilation(V)shouldideallymatchperfusion(Q)atthealveolar-
capillarylevel.Areasofventilationwithoutperfusionaretermeddeadspace(e.g.,pulmonary
embolus).
• Diffusionabnormality:abnormalityofthealveolar-capillarymembranecausinginefcientexchange
ofoxygentothebloodstream(e.g.,diseasesofthelungparenchymaorinterstitium)

CHAPTER 17 RESPIRATORYDISORDERS 187
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30. What causes stridor?
Stridor,anairwayemergencythatdemandsimmediateattention,iscausedbypartialobstruction
oftheairwayatthelevelofthelarynxortrachea.Thishigh-pitchedbreathsoundcanbenotedon
inspirationorexpirationorcanevenbebiphasic.
31. What is the definition of acute respiratory failure?
RespiratoryfailureisaninadequateexchangeofO2andCO2secondarytofailureoftheventilatory
apparatusorgasexchangesystem.Itresultsinhypoventilationand,therefore,hypercapniaand
hypoxemia.
32. How is the diagnosis of respiratory failure made?
RespiratoryfailureisprimarilybasedonABGs:hemoglobinsaturationof<92%(whichcorrespondsto
aPaO2of<60mmHg,aPaCO2of>50mmHg,andapHof<7.35[respiratoryacidosis]).
33. How is respiratory failure treated?
SecureandmaintainapatentairwaytodeliverappropriateO2therapyusingmechanicalorsupportive
ventilation.Theairwaymaybeintheformoforalandnasalendotrachealintubation,tracheostomy,or
cricothyrotomy.
34. What are the indications for elective intubation and mechanical ventilation?
Theindicationsforintubationandmechanicalventilationarebasedonclinicalandlabvalues.These
include:
• Respiratoryrate>30to40breaths/min
• Negativeinspiratorypressure<25cmH2O
• Vitalcapacity<10to15mL/kgoraPaCO2>50mmHgwithapH<7.3
35. What are the guidelines for withdrawing mechanical ventilatory support (weaning
parameters)?
Mechanicalventilationcanbewithdrawnifoneormoreofthefollowingparametersaremet:
• PaO2>60mmHgwithanFiO2<0.4
• Minuteventilation<10L/min
• PaCO2(35to45)acceptablewithnormalpH
• Respiratoryrate<25breaths/min
• Tidalvolume>4to5mL/kg
• Negativeinspiratorypressure>20cmH2O
• Vitalcapacity>10to15mL/kg
36. What is pleural effusion?
Pleuraleffusionoccurswhenuidaccumulatesinthepleuralspace(i.e.,volumeoverload,infection)
andtheair-lledlungseparatesfromthechestwall.
37. What is atelectasis?
Atelectasisoccurswhenmucusoraforeignobjectobstructsairowinamainstembronchuscausing
collapseoftheaffectedlungtissueintoanairlessstate.Ittypicallyoccurs36hourspostoperatively
andpresentswithmilddyspnea.
38. What chest X-ray findings are noted in a patient with atelectasis?
Radiologicsignsoflobaratelectasiscanbecategorizedasdirectorindirect.Directsignsinclude
increasedopacicationoftheairlesslobeanddisplacementofssures.Indirectsignsinclude
displacementofhilarandcardiomediastinalstructurestowardthesideofcollapse,narrowingofthe
ipsilateralintercostalspaces,elevationoftheipsilateralhemidiaphragm,compensatoryhyperination
andhyperlucencyoftheremainingaeratedlung,andobscurationofthestructuresadjacenttothe
collapsedlung.
39. How is postoperative atelectasis managed?
Treatmentofpostoperativeatelectasisisaimedatexpansionofthelung,and,formostpatients,
incentivespirometryisadequate.However,inpatientswithsevereatelectasis,endotrachealsuction
andevenbronchoscopymaybewarranted.
40. What are the signs of pneumothorax?
Pneumothoraxoccurswhenairleaksintothepleuralspace,causingthelungtorecoilfromthechest
wall.Thesignsofintraoperativepneumothoraxincludeunexplainedhypotension,ventilatoryhypoxiawith

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bulgingdiaphragm,jugularvenousdistention,tympanicthorax,andtracheadeviatedtooneside.Inan
awakepatient,apneumothoraxtypicallypresentswithdyspnea,chestpain,absenceofbreathsounds
ontheaffectedside,andevidenceofpneumothoraxonchestX-ray.Trachealdeviationmaybepresent.
41. What is the appropriate treatment of pneumothorax?
Pneumothoraxisdenitivelytreatedwithplacementofathoracostomytubeconnectedtoclosed
suctionof20cmH2O.However,iftensionpneumothoraxissuspected,immediateneedledecompres-
sionthroughthesecondintercostalspaceinthemidclavicularlineusinga14-gaugeneedleshouldbe
performed.
42. What is the mechanism of bronchial asthma?
Asthmaisachronicdisordercharacterizedbyinammationandincreasedresponsivenessofthe
tracheobronchialtreetodiversestimuliresultinginavaryingdegreeofairwayobstruction.
43. What is the clinical presentation of bronchial acute asthma?
Patientspresentwithdyspneaortachypnea,wheezing,hypoxemia,and,occasionally,hypercapnia.
44. How is bronchial asthma classified?
Oneoftheclassicationsofasthmaisbasedontheseverityandfrequencyofattack(Table17-1).
45. What is the appropriate management of an acute asthma attack?
AnacuteasthmaticattackisbesttreatedbyadministrationofsupplementalO2withaninhaledbeta-
adrenergicagonist(albuterol,3.0mL[2.5mg],in2mLofnormalsalineevery4to6hours,inanebulizer).
Ifthepatientisresistanttobetaagonists,theophyllineshouldbeconsidered.Therapyalsomayinclude
parenteralsteroids,suchasmethylprednisolone(50to250mgover4to6hours).Inasevereasthmatic
attackthatisunresponsivetotheabove,administer0.3mgof1:1000epinephrinesubcutaneously.
46. What clinical information is relevant for patients with COPD to risk-stratify prior to
surgery?
• Smokinghistory:numberofpacksperdaysanddurationinyears
• Clinicalsymptoms:dyspnea,wheezing,cough
• Functionalcapacity:assessmentofmetabolicequivalents(METs).Thosewhocannottolerate>4
METs(i.e.,climbing≥1ightofstairs,walkingonetotwoblocksuphill,golf)areconsidered
increasedrisk.
• Hospitalizations:previousintubations/needformechanicalventilation
• Medications:homeO2therapyandow-rate?Needforsystemicsteroids?
• Infections:anyrecentexacerbations,pulmonaryinfections
• Weightloss:mayberelatedtoend-stagelungdiseaseorcancer
47. What is emphysema?
Emphysemaisaninammatoryresponseinthelungsduetocontinuousexposuretoirritantssuchas
airpollutionandsmoking.Thiscausesnarrowingofsmallairwaysandbreakdownofthelungtissue
resultingindestructionofairspaces.Theresultantbrosisresultsinairtrapping(hyperination)and
ventilation-perfusionmismatch.Patientscompensatethroughhyperventilationandprolongedexpiratoryperiodstomaintainoxygensaturation>90%(i.e.,pinkpuffer).Physicalexaminationrevealsuse
ofaccessorymuscles,hyperinatedlungeldsthatarehyperresonanttopercussion,withdistant,
diminishedbreathsounds.
Table 17-1. Classifying the Severity of an Asthma Attack
SEVERITY
Intermittent ≤2/week ≤2/month ≥80% ≤2days/week
Mild persistent >2/week 3-4/month ≥80% >2days/week
Moderate
persistent
Severe persistent Continuously Frequent(7/week) <60% ≥2/day
SYMPTOM
FREQUENCY
Daily >1/week 60-80% Daily
NIGHTTIME
SYMPTOMS
% FEV1 OF
PREDICTED
SHORT-ACTING
BETA-AGONIST
USE

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48. What is chronic bronchitis?
Chronicproductivecoughlastingatleast3monthsoveraminimumof2yearsthatishighlyassoci-
atedwithsmoking.Itischaracterizedbyhypertrophyofbronchialmucinousglands.Thishypertrophy
leadstoincreasedthicknessofmucusglandsrelativetooverallbronchialwallthickness(Reidindex
increasesto>50%;normalis<40%).Theclinicalsignsareaproductivecough(duetoexcessive
mucusproduction)andcyanosis(bluebloaters).Theexcessmucuscausesmucousplugs,trapping
carbondioxide,increasingPaCO2,anddecreasingPaO2,resultinginanincreasedriskofinfectionand
corpulmonale.
49. What is bronchiectasis?
Bronchiectasisisaconditioninwhichthebronchiareabnormallyandirreversiblydilateddueto
destructionofthemuscleandelasticityofthelungparenchymasecondarytoinammation.The
disordercanbeassociatedwithcongenitallungdiseasesortheresultofavarietyofpulmonary
insultsincludingaspirationorsevereinfection.Theresultantdilationanddestructioncausesthelung
toinadequatelyclearsecretionsandbecomecolonizedwithpathogenicbacteria,resultinginrecurrent
pulmonaryinfections.
50. What is adult respiratory distress syndrome (ARDS)?
ARDSisaC5a-inducedneutrophilaggregationinthelung.Thisaggregationisoneofthemajor
mechanismsofpathologyofARDS.Thedamagedcapillariesleakprotein-richuidintotheinterstitium,whichleadstochangesinpulmonaryfunction.
51. What causes ARDS?
ARDSusuallyresultsfromaninjurytothealveolar-capillarymembrane.Italsocanbecausedby
anexistingunderlyingdisease,suchassystemicsepsis,fatembolism,headinjury,aspiration,
pancreatitis,orinhalationinjury.Patientstypicallyshowseveredyspneaandhypoxemiarefractoryto
supplementalO2withdiffusepulmonaryinltratesonchestradiograph.
52. What is the appropriate management of ARDS?
ManagementofARDSincludesimmediatetransfertoanintensivecareunitandplacementofa
pulmonaryarterycatheterwithmechanicalventilationtomaintainthepulseoximetry(SpO2)>90%,
whichcorrespondstoPO2>60mmHg.Inaddition,thepulmonarycapillarypressureshouldbekeptin
therangeof12to15mmHg,andthecardiacindexshouldbemaintainedabove3L/min/m2.TreatmentofARDSisgenerallysupportivetoachieveO2saturationof90%whileminimizingbarotrauma
andoxygentoxicity.
53. What are the features of ARDS?
• Historyofmajorinsult
• Increasedrespiratorydistress
• DiffuseinltrationonchestX-ray
• Hypoxemia(PaO2<60mmHgwithFiO2>0.6)
• Respiratoryalkalosis
• Normalpulmonarycapillarywedgepressure(PCWP)
• Decreasedpulmonarycompliance
• Increasedshuntfunction
• Increaseddeadspaceandventilation
54. How often does aspiration occur, and what are the complications?
Aspirationisarelativelyrareoccurrenceaffectingapproximately1outofevery10,000patients
undergoinggeneralanesthesia.Intheoutpatientsetting,deepsedationwithoutasecureairwayhas
alsobeenshowntobesafewithoutasignicantincreasedriskforaspiration.Complicationsinclude
bronchospasm,pneumonitis,pneumonia,acuterespiratorydistresssyndrome,lungabscess,and
empyemaconferringanincreasedriskofmortality.
55. What are common risk factors for aspiration?
• InadequateNPOstatus(emergentcases)orfailuretofollowNPOguidelinesforanesthesia
• Extremesofage(twiceascommoninchildrenandelderly)
• Medicationsthatdecreaselevelofconsciousness(sedative/hypnotics/anxiolytics)andbluntprotec-
tivereexes
• Headtrauma
• Stroke

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• Presenceofanasogastrictube
• Prolongedsupineposition
56. What is the appropriate management of aspiration?
Abaselinechestradiographshouldbeobtainedforanypatientsuspectedofaspiration.Afterimme-
diatesuctioning,supportivecareisthemainstayoftreatmentandincludessupplementaloxygen
andmonitoringofoxygensaturationinaninpatientsetting.Ventilatorysupportshouldbeinitiated
ifconcernforrespiratoryfailurearises(seequestion12above).Antibioticsshouldnotbeinitiated
unlesstheeventleadstopneumoniaandculturescanbetailoredtotargetspecicorganisms.
Classically,aspiratedmaterialconsistsofgram-negativeoranaerobicorganisms(oral/gastrointestinalora).Aspirationofgastriccontentscanleadtochemicalpneumonitisandalsorequires
supportivecare.
57. How can aspiration risk be decreased?
Byrecognizingsurgicalpatientswhoarehighrisk,adjunctivestepsandmedicationcanbetakento
minimizetheoverallrisk.Adheringtostandardfastingprotocolspriortoanyprocedurewilloptimize
gastricemptying.Gastricacidscanbeneutralizedwithantacidsorhistaminereceptorantagonists.
Logically,pro-motilityagentssuchasmetoclopramidewillaidingastricemptying;however,nodata
supportsthis.Aspirationcanbepreventedincriticallyillpatientsbymaintainingthehead-of-bed
≥30degrees,minimizingsedatives,andavoidingbolusfeedsinhigh-riskpatients.
58. What drugs interfere (interact) with aminophylline?
Themostcommonlyciteddrugiserythromycin,whichincreasesserumlevelsofaminophylline.
Cimetidinealsoincreasesserumlevelsofaminophylline.
59. What are the signs and symptoms of pulmonary embolism (PE)?
PEcanpresentwithacuteonsetofpleuriticchestpain,dyspnea,syncope,orlegpainandswelling.
Manypatientsmayhavenosymptoms.SignsofaPEincludetachypnea,hypoxemia,rales,unexplainedtachycardia,elevatedjugularvenouspressure,andlow-gradefever.RiskfactorsforPEinclude
stasis(immobility,obesity),recentendothelialinjury(trauma,surgery,recentfracture,anddeepvein
thrombosis),andhypercoagulablestate(pregnancy,oralcontraceptiveuse,malignancy).
60. How is the pre-test probability of deep vein thrombosis (DVT) determined?
TheWell’scriteriaisamethodofdeterminingthelikelihoodofDVT.Itisbasedonmajorandminor
criteria.Majorcriteriaincludeactivecancer,immobilization,bedrest>3days,majorsurgerywithin
4weeks,swellingofthethighandcalf,familyhistoryofDVT.Minorcriteriaincluderecenttraumato
symptomaticextremitywithin60days,pittingedema,dilatedsupercialveins,erythema,andrecent
hospitalizationwithin6months.Ifmorethanthreemajorcriteriaortwomajorandtwominorcriteria
aremet,thenthereisahighlikelihoodthatDVT/PEcanbepresent(∼85%+DVT).
61. How is PE diagnosed?
ImmediateABG,electrocardiogram(ECG),andchestX-rayshouldbeobtained.TheABGwill
revealhypoxemia,hypocapnia,andrespiratoryalkalosiswithanincreasedA–agradient.AnECG
mayrevealsinustachycardiaoratrialbrillationwithsignsofrightventricularstrain(e.g.,right
bundlebranchblockwitht-waveinversionsinleadsV1-V4).ChestX-raymayshowatelectasis,
effusion,andaraiseddiaphragm.WithalargePE,thechestX-raymayhaveaHamptom’shump,a
wedge-shapeddensityabuttingthepleura,orWestermarksign,whichsharplycutsoffofavessel
distaltotheembolus.D-dimerlevelscanbeassessedwithhighsensitivitybutpoorspecicity.If
thepatientisexperiencinganyasymmetricswellinginanyextremity,thenDVTshouldberuled
outwithanultrasound.BypassingtheselaboratorytestsandobtainingCTangiographymaybe
warranted.
62. What is the appropriate management of postoperative PE?
Oncethepatienthasbeenstabilized,treatmentincludesacuteanticoagulationwithintravenousor
subcutaneousheparinoralowmolecularweightheparin.Ifgivenintravenously,heparinshouldbe
titratedtoagoalPTTof60to85seconds.Oncesuitableacuteanticoagulationhasoccurredand
PTTistherapeutic,thepatientistransitionedtoanticoagulationwithwarfarin(goalINRof2to3for
3to6monthspostevent).Withacontraindicationforanticoagulation,aninferiorvenacavalter
shouldbeplaced.ForlargeproximalPEwithhemodynamiccompromise,thrombectomymaybe
considered.

CHAPTER 17 RESPIRATORYDISORDERS 191
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BiBliography
BarashP,CullenB,StoeltingR,etal.:Clinical anesthesia,ed2,Philadelphia,1996,Lippincott-Raven.
BatesB,BickleyL,HoekelmanR:Thethoraxandlungs.InBatesB,editor:A guide to physical examination and history
taking,ed6,Philadelphia,1995,J.B.Lippincott.
BradleyTD,RutherfordR,GrossmanRF,etal.:Roleofdaytimehypoxemiainthepathogenesisofrightheartfailureinthe
obstructivesleepapneasyndrome,Am Rev Respir Dis131:835,1985.
ChungF,YangY,LiaoP:PredictiveperformanceoftheSTOP-Bangscoreforidentifyingobstructivesleepapneainobese
patients,Obes Surg23(12):2050–2057,December2013.
CohenMM,DuncanPG,PopeWD,WolkensteinC:Asurveyof112,000anaestheticsatoneteachinghospital(1975–83),
Can Anaesth Soc J33:22–31,1986.
DeanG,JacobsAR,GoldsteinRC,GevirtzCM,PaulME:Thesafetyofdeepsedationwithoutintubationforabortioninthe
outpatientsetting,J Clin Anes23:437–442,2011.
GottliebDJ,YenokyanG,NewmanAB,etal.:Prospectivestudyofobstructivesleepapneaandincidentcoronaryheart
diseaseandheartfailure:thesleephearthealthstudy,Circulation122:352,2010.
KearneyDJ,LeeTH,ReillyJJ,etal.:Assessmentofoperativeriskinpatientsundergoinglungresection,importanceof
predictedpulmonaryfunction,Chest105:753–759,1994.
KispertJF,KazmersA,RoimanL:Preoperativespiromterypredictspredictsperioperativepulmonarycomplicationsafter
majorvascularsurgery,Ann Surg58:491–495,1992.
KollefM,GoodenbergerD:Criticalcareandmedicalemergencies.InEwaldG,McKenzieC,editors:The Washington manual
of medical therapeutics,Boston,1995,Little,Brown.
LiKK:MaxillomandibularAdvancementforobstructivesleepapnea,J Oral Maxillofac Surg69(3):687–694,March2011.
EpubDecember24,2010.
Martínez-GarcíaMA,Campos-RodríguezF,Catalán-SerraP,etal.:Cardiovascularmortalityinobstructivesleepapnea
intheelderly:roleoflong-termcontinuouspositiveairwaypressuretreatment:aprospectiveobservationalstudy,
Am J Respir Crit Care Med186:909,2012.
MillerR,StoeltingR:Acid-baseandbloodgasanalysis.InMillerR,editor:Basics of anesthesia,ed3,NewYork,1994,
ChurchillLivingstone.
MillerWP:Cardiacarrhythmiasandconductiondisturbancesinthesleepapneasyndrome.Prevalenceandsignicance,
Am J Med73:317,1982.
MurrayMJ,CoursinDB,PearlRG,ProughDS:Critical care medicine perioperative management,ed2,Philadelphia,2002,
Lippincott.
NationalAsthmaEducationandPreventionProgram:Expert panel report III: guidelines for the diagnosis and management
of asthma,Bethesda,MD,2007,NationalHeart,Lung,andBloodInstitute(NIHpublicationno.08-4051).
www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.
OlssonGL,HallenB,Hambraeus-JonzonK:Aspirationduringanaesthesia:acomputer-aidedstudyof185,358anaesthet-
ics,Acta Anaesthesiol Scand30:84–92,1986.
PettitTW,CobbJP:Criticalcare.InDohertyGM,WellsSA,BaumannDS,etal.:The Washington manual of surgery,Boston,
1997,Little,Brown.
PunjabiNM,CaffoBS,GoodwinJL,etal.:Sleep-disorderedbreathingandmortality:aprospectivecohortstudy,PLoS Med
6:e1000132,2009.
RoserSM:Managementofthemedicallycompromisedpatient.InKwonP,LaskinD,editors:Clinician’s manual of oral and
maxillofacial surgery,ed2,Chicago,1997,Quintessence.
VanaKD,SilvaGE,GoldbergR:PredictiveabilitiesoftheSTOP-BangandEpworthSleepinessScaleiniden-
tifyingsleepclinicpatientsathighriskforobstructivesleepapnea,Res Nurs Health36:84–94,2013,
http://dx.doi.org/10.1002/nur.21512.
WellsPS,etal.:Derivationofasimpleclinicalmodeltocategorizepatientswithaprobabilityofpulmonaryembolism:
increasingthemodelsutilitywiththeSimpliREDD-dimer,Thromb Haemost83(3):416–420,2000.
WellsPS,etal.:Excludingpulmonaryembolismatthebedsidewithoutdiagnosticimaging:managementofpatientswith
suspectedpulmonaryembolismpresentingtotheemergencydepartmentbyusingasimpleclinicalmodelandd-dimer,
Ann Intern Med135(2):98–107,2001.
WestJB:Respiratory physiology: the essentials,ed9,Baltimore,2012,Lippincott,Williams,andWilkins.
WestJB:Pulmonary pathophysiology: the essentials,ed8,Baltimore,2012,Lippincott,Williams,andWilkins.
YoungT,FinnL,PeppardPE,etal.:Sleepdisorderedbreathingandmortality:eighteen-yearfollow-upoftheWisconsin
sleepcohort,Sleep31:1071,2008.
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