Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 952 - файл

.pdf
Скачиваний:
0
Добавлен:
29.08.2026
Размер:
7 Мб
Скачать
182 PART IV MANAGEMENT CONSIDERATIONS
https://t.me/medicina_free
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)
RESPIRATORYDISORDERS
https://t.me/medicina_free
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?
• AlowpHorahighPCO2shiftsthecurvetotheright.  • AhighpHoralowPCO2shiftsthecurvetotheleft.  • Elevatedbodytemperatureshiftsthecurvetotheright.  • Lowerbodytemperatureshiftsthecurvetotheleft.  • Carbonmonoxideinthebloodincreasestheafnityofremainingoxygenforhemoglobinandshifts
thecurvetotheleft.
3. How does the interpretation of the curve change when the curve shifts to the left?
TheP50isaconventionalmeasureofthehemoglobinafnityforoxygen.Ifthecurveisshiftedto
theleft,thereislessPO2(mmHg)inthebloodneededtoachievetheP50.Inotherwords,thereisan increasedhemoglobinafnitytoO2withaleftcurveshift.
4. What is 2,3-diphosphoglycerate (2,3-DPG)?
Itisproducedbyerythrocytesandnormallyispresentinfairlyhighconcentrationsinredbloodcells
(RBCs).
5. When is 2,3-DPG produced?
Itisproducedmainlyduringchronichypoxicconditions.Anincreasein2,3-DPGshiftsthecurvetothe
rightandallowsmoreO2tobereleasedfromhemoglobinataparticularO2level.Withadecreasein 2,3-DPG,thecurvewillshifttotheleft,indicatinganincreasedafnityforO2byhemoglobin.Hemo­globindoesnotreleaseO2inthetissuesexceptataverylowPO2.
6. How does 2,3-DPG affect blood supply in blood banks?
Bloodstoredforaslittleas1weekwillhavedepleted2,3-DPGunlessstepsaretakentorestore
normallevelsof2,3-DPG.
7. How does the aging process affect PaCO2?
PaCO2andalveolarventilationareunchangedbytheagingprocess.
8. How does the aging process affect PaO2?
PaO2decreaseswithage.Thisdecreasecanbecalculatedaccordingtothefollowingformula:
CHAPTER 17
ThusthePaO2ofa30-year-oldpersonwouldbecalculatedas100.1−(0.323×30)=90.41.
9. What are the anatomic volumes of the lungs?
TV:tidalvolume,theamountofairmovedwitheachbreath(Fig. 17-2) IRV:inspiratoryreservevolume,themaximumadditionalamountofairthatcanbeinhaledafterthe
endofinspiration IC:inspiratorycapacity,themaximumvolumeofairthatcanbeinspired(VT+IRV) RV:residualvolume,theremainingvolumeofairaftermaximalexpiration ERV:expiratoryreservevolume,themaximumadditionalamountofairthatcanbeexhaledafter
expiration FRC:functionalresidualcapacity,thevolumeinthelungsafterpassiveexpiration(RV+ERV) VC:vitalcapacity,themaximumamountofairthatcanbeexhaledaftermaximuminspiration
(IC+ERV) TLC:totallungcapacity,thevolumeinthelungsatmaximalinspiration(RV+VC)
183
184 PART IV MANAGEMENTCONSIDERATIONS
6000mL
Time
https://t.me/medicina_free
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. Normaloxyhemoglobindissociationcurve.DPG,Diphosphoglycerate;COHb,carboxyhemoglobin;Hb,hemo­globin. (From Cairo JM, Pilbeam SP: Mosby’srespiratorycareequipment, 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. Lungvolumesandcapacities. (From Nagelhout JJ, Plaus K: Nurseanesthesia, ed 4, St Louis, 2010, Saunders.)
CHAPTER 17 RESPIRATORYDISORDERS 185
https://t.me/medicina_free
10. What are pulmonary function tests (PFTs), and why are they used?
PFTsareanadjuncttohistoryandphysicalexaminationandprovideanoverallassessmentofthe
respiratorysystem.Thetestsinclude(1)measurementsofairow(spirometry),(2)lungvolumes,and (3)diffusingcapacityforinspiredcarbonmonoxide(DLCO).Thetestsarereportedasapercentageof predictednormalvaluesbasedonageandheight.
11. What useful measurements are used in spirometry?
FVC:Forcedvitalcapacity FEV1:thevolumeofairthatcanforciblybeblownoutin1second,afterfullinspiration FVC/FEV1ratio:knownastheTiffeneau-Pinellindex
12. What is the normal FVC/FEV1 ratio?
ThenormalFVC/FEV1ratiois70%to80%.
13. What is the FVC/FEV1 ratio in obstructive and restrictive disease?
Inobstructivepulmonarydisease,expiratoryresistanceincreases,resultinginanincreaseintheFEV1.
TheFVCmayalsoincrease,butnottothesameextent,resultinginadecreasedratiobelow70%.In restrictivediseasesuchaspulmonarybrosis,theFVCandtheFEV1arebothreducedproportionally, resultinginanormalratioorevenincreasedasaresultofdecreasedlungcompliance.
14. How is the forced expiratory volume in 1 second (FEV1) changed with age?
FEV1declineslinearlywithageincrease.
15. What are the most significant changes of pulmonary function associated with aging?
• Lossoflungelasticity,whichleadstoincreasedmeanalveolardiameterandvolumeandreducedFEV  • Decreasedpoweroftherespiratorymusculature
1
• Increasedrigidityofribcage Allthesechangesstartbecomingapparentinthethirddecadeoflife.
16. What is the normal rate of breathing?
Thenormalrespiratoryrate(RR)is10to20breaths/mininadolescentsandadults(>12yearsold),
30to60ininfants(0to1year),24to40intoddlers(1to3years),22to34inthose3to6yearsold, and18to30inthose6to12yearsold.Foradolescentsandadults,anRR>20/minisconsidered tachypneaand<10/minisbradypnea.
17. Where is the respiratory center?
Therespiratorycenterisawidelydispersedgroupofneuronslocatedbilaterallyinthereticular
substanceofthemedullaoblongataandpons.
18. What influences the respiratory center?
ExcessCO2andhydrogenions(H+)affectrespirationmainlybydirectexcitatoryeffectsontherespi-
ratorycenteritself.Oxygendoesnothaveasignicantdirecteffectontherespiratorycenter.O2acts almostentirelyperipherallyonthecarotidandaorticbodies.
19. What does PEEP mean?
PositiveEnd-ExpiratoryPressureduringmechanicalventilation.PEEPaidsinpreventingalveolarand
smallairwaycollapseandmayhelprecruitlungunitsthatwerepreviouslycollapsed.
20. What are the beneficial effects of PEEP?
• Increasedfunctionalresidualcapacity  • Increasedcompliance  • IncreasedPaO  • Increasedventilation–perfusion(V/Q)ratio(wheninitiallylow)
2
• Decreasedpulmonaryshunt
21. What is the effect of PEEP on cardiac output?
BecauseofincreasedintrathoracicpressureanddecreasedvenousreturnwhenusingPEEP,cardiac
outputmaybedecreased.
22. What are the normal blood gas values?
pH7.40±0.05units (H+)40±5mEq/L
186 PART IV MANAGEMENTCONSIDERATIONS
https://t.me/medicina_free
PCO240±5mmHg
A0.1decreaseinpHcorrespondstoa12mmHgofPCO2increase,whichequalsabasechangeof6mEq/L.  • Goldenruleno.1:ApHof0.08=PaCO2of10mmHg.  • Goldenruleno.2:ApHof0.15=basechangeof10mEq/L.
23. What are the common causes of acid–base disorders?
• Respiratoryalkalosis:hyperventilation,sepsis,anxiety,pain  • Respiratoryacidosis:CNSdepression,neuromusculardisorders,upperandlowerairway
abnormalities
• Metabolicalkalosis:emesis,volumedepletion,nasogastrictube(NGT)drainage,diureticuse,
exogenousalkali,mineralocorticoidexcess
• Metabolicacidosis:ketoacidosis,lacticacidosis,renalfailure,ingestionoftoxins(e.g.,methanol
andpropyleneglycol)
24. How is the diagnosis of respiratory acidosis made?
Respiratoryacidosisisusuallyevidentfromtheclinicalexam,especiallyifrespirationisobviously
depressed.Analysesofarterialbloodgases(ABGs)willconrmthediagnosis.ArterialpHwillbe <7.35,andPCO2willbe>45mmHg.
25. What are some causes of respiratory acidosis?
Anydiseaseorconditionthatmayaffecttherespiratoryfunctioncancauserespiratoryacidosis,
including:
• Chronicobstructivepulmonarydisease(COPD)  • Chestwallorairwayinjury  • Drugeffects  • Pulmonaryedema  • Centralnervoussystem(CNS)depression  • Cardiacarrest  • Extremeobesity(e.g.,pickwickiansyndrome)  • Pneumonia
26. How is the diagnosis of respiratory alkalosis made?
Clinically,respiratoryalkalosisusuallymanifestsashyperventilation.However,dependingonitssever-
ityandacuteness,hyperventilationmaynotbeevident,butananalysisofABGswilldemonstratean arterialpHof>7.45andaPCO2of<35mmHg.
27. What are some causes of respiratory alkalosis?
• Hyperventilation  • Pulmonaryembolus  • CNSinjury  • Excessivemechanicalventilation  • Fever
28. What is Cheyne-Stokes breathing?
Periodsofhyperpnea(deepbreathing)alternatingwithperiodsofapnea.Thecrescendo–decrescendo
patternofbreathingisassociatedwithchangesinPO2andPCO2.Childrenandtheelderlynormally showthispatterninsleep.Innormaladults,causesofthispatternofbreathingincludeheartfailure, uremia,drug-inducedrespiratorydepression,andbraindamage.
29. What are the causes of hypoxemia?
• Lowinspiredoxygenconcentration(lowFiO2):wheninadequateoxygenlevelissuppliedoravail-
able(e.g.,asphyxiation)  • Hypoventilation:inadequateminuteventilation(e.g.,sedationorCNSdepression,brainstemstroke)  • Righttoleftshunt:perfusionwithoutventilation;whenbloodbypassesthepulmonarysystemby
owingfromtherighthearttotheleftwithoutexposuretoinhaledoxygen(e.g.,atrialorventricular
septaldefect,pulmonaryedema,pneumonia)  • Ventilation/perfusionmismatch:Ventilation(V)shouldideallymatchperfusion(Q)atthealveolar-
capillarylevel.Areasofventilationwithoutperfusionaretermeddeadspace(e.g.,pulmonary
embolus).  • Diffusionabnormality:abnormalityofthealveolar-capillarymembranecausinginefcientexchange
ofoxygentothebloodstream(e.g.,diseasesofthelungparenchymaorinterstitium)
CHAPTER 17 RESPIRATORYDISORDERS 187
https://t.me/medicina_free
30. What causes stridor?
Stridor,anairwayemergencythatdemandsimmediateattention,iscausedbypartialobstruction
oftheairwayatthelevelofthelarynxortrachea.Thishigh-pitchedbreathsoundcanbenotedon inspirationorexpirationorcanevenbebiphasic.
31. What is the definition of acute respiratory failure?
RespiratoryfailureisaninadequateexchangeofO2andCO2secondarytofailureoftheventilatory
apparatusorgasexchangesystem.Itresultsinhypoventilationand,therefore,hypercapniaand hypoxemia.
32. How is the diagnosis of respiratory failure made?
RespiratoryfailureisprimarilybasedonABGs:hemoglobinsaturationof<92%(whichcorrespondsto
aPaO2of<60mmHg,aPaCO2of>50mmHg,andapHof<7.35[respiratoryacidosis]).
33. How is respiratory failure treated?
SecureandmaintainapatentairwaytodeliverappropriateO2therapyusingmechanicalorsupportive
ventilation.Theairwaymaybeintheformoforalandnasalendotrachealintubation,tracheostomy,or cricothyrotomy.
34. What are the indications for elective intubation and mechanical ventilation?
Theindicationsforintubationandmechanicalventilationarebasedonclinicalandlabvalues.These
include:  • Respiratoryrate>30to40breaths/min  • Negativeinspiratorypressure<25cmH2O  • Vitalcapacity<10to15mL/kgoraPaCO2>50mmHgwithapH<7.3
35. What are the guidelines for withdrawing mechanical ventilatory support (weaning
parameters)?
Mechanicalventilationcanbewithdrawnifoneormoreofthefollowingparametersaremet:  • PaO2>60mmHgwithanFiO2<0.4  • Minuteventilation<10L/min  • PaCO2(35to45)acceptablewithnormalpH  • Respiratoryrate<25breaths/min  • Tidalvolume>4to5mL/kg  • Negativeinspiratorypressure>20cmH2O  • Vitalcapacity>10to15mL/kg
36. What is pleural effusion?
Pleuraleffusionoccurswhenuidaccumulatesinthepleuralspace(i.e.,volumeoverload,infection)
andtheair-lledlungseparatesfromthechestwall.
37. What is atelectasis?
Atelectasisoccurswhenmucusoraforeignobjectobstructsairowinamainstembronchuscausing
collapseoftheaffectedlungtissueintoanairlessstate.Ittypicallyoccurs36hourspostoperatively
andpresentswithmilddyspnea.
38. What chest X-ray findings are noted in a patient with atelectasis?
Radiologicsignsoflobaratelectasiscanbecategorizedasdirectorindirect.Directsignsinclude
increasedopacicationoftheairlesslobeanddisplacementofssures.Indirectsignsinclude
displacementofhilarandcardiomediastinalstructurestowardthesideofcollapse,narrowingofthe
ipsilateralintercostalspaces,elevationoftheipsilateralhemidiaphragm,compensatoryhyperination
andhyperlucencyoftheremainingaeratedlung,andobscurationofthestructuresadjacenttothe
collapsedlung.
39. How is postoperative atelectasis managed?
Treatmentofpostoperativeatelectasisisaimedatexpansionofthelung,and,formostpatients,
incentivespirometryisadequate.However,inpatientswithsevereatelectasis,endotrachealsuction
andevenbronchoscopymaybewarranted.
40. What are the signs of pneumothorax?
Pneumothoraxoccurswhenairleaksintothepleuralspace,causingthelungtorecoilfromthechest
wall.Thesignsofintraoperativepneumothoraxincludeunexplainedhypotension,ventilatoryhypoxiawith
188 PART IV MANAGEMENTCONSIDERATIONS
https://t.me/medicina_free
bulgingdiaphragm,jugularvenousdistention,tympanicthorax,andtracheadeviatedtooneside.Inan
awakepatient,apneumothoraxtypicallypresentswithdyspnea,chestpain,absenceofbreathsounds
ontheaffectedside,andevidenceofpneumothoraxonchestX-ray.Trachealdeviationmaybepresent.
41. What is the appropriate treatment of pneumothorax?
Pneumothoraxisdenitivelytreatedwithplacementofathoracostomytubeconnectedtoclosed
suctionof20cmH2O.However,iftensionpneumothoraxissuspected,immediateneedledecompres-
sionthroughthesecondintercostalspaceinthemidclavicularlineusinga14-gaugeneedleshouldbe
performed.
42. What is the mechanism of bronchial asthma?
Asthmaisachronicdisordercharacterizedbyinammationandincreasedresponsivenessofthe
tracheobronchialtreetodiversestimuliresultinginavaryingdegreeofairwayobstruction.
43. What is the clinical presentation of bronchial acute asthma?
Patientspresentwithdyspneaortachypnea,wheezing,hypoxemia,and,occasionally,hypercapnia.
44. How is bronchial asthma classified?
Oneoftheclassicationsofasthmaisbasedontheseverityandfrequencyofattack(Table17-1).
45. What is the appropriate management of an acute asthma attack?
AnacuteasthmaticattackisbesttreatedbyadministrationofsupplementalO2withaninhaledbeta-
adrenergicagonist(albuterol,3.0mL[2.5mg],in2mLofnormalsalineevery4to6hours,inanebulizer).
Ifthepatientisresistanttobetaagonists,theophyllineshouldbeconsidered.Therapyalsomayinclude
parenteralsteroids,suchasmethylprednisolone(50to250mgover4to6hours).Inasevereasthmatic
attackthatisunresponsivetotheabove,administer0.3mgof1:1000epinephrinesubcutaneously.
46. What clinical information is relevant for patients with COPD to risk-stratify prior to
surgery?
• Smokinghistory:numberofpacksperdaysanddurationinyears  • Clinicalsymptoms:dyspnea,wheezing,cough  • Functionalcapacity:assessmentofmetabolicequivalents(METs).Thosewhocannottolerate>4
METs(i.e.,climbing1ightofstairs,walkingonetotwoblocksuphill,golf)areconsidered
increasedrisk.  • Hospitalizations:previousintubations/needformechanicalventilation  • Medications:homeO2therapyandow-rate?Needforsystemicsteroids?  • Infections:anyrecentexacerbations,pulmonaryinfections  • Weightloss:mayberelatedtoend-stagelungdiseaseorcancer
47. What is emphysema?
Emphysemaisaninammatoryresponseinthelungsduetocontinuousexposuretoirritantssuchas
airpollutionandsmoking.Thiscausesnarrowingofsmallairwaysandbreakdownofthelungtissue resultingindestructionofairspaces.Theresultantbrosisresultsinairtrapping(hyperination)and ventilation-perfusionmismatch.Patientscompensatethroughhyperventilationandprolongedexpira­toryperiodstomaintainoxygensaturation>90%(i.e.,pinkpuffer).Physicalexaminationrevealsuse ofaccessorymuscles,hyperinatedlungeldsthatarehyperresonanttopercussion,withdistant, diminishedbreathsounds.
Table 17-1. Classifying the Severity of an Asthma Attack
SEVERITY
Intermittent 2/week 2/month 80% 2days/week Mild persistent >2/week 3-4/month 80% >2days/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
CHAPTER 17 RESPIRATORYDISORDERS 189
https://t.me/medicina_free
48. What is chronic bronchitis?
Chronicproductivecoughlastingatleast3monthsoveraminimumof2yearsthatishighlyassoci-
atedwithsmoking.Itischaracterizedbyhypertrophyofbronchialmucinousglands.Thishypertrophy leadstoincreasedthicknessofmucusglandsrelativetooverallbronchialwallthickness(Reidindex increasesto>50%;normalis<40%).Theclinicalsignsareaproductivecough(duetoexcessive mucusproduction)andcyanosis(bluebloaters).Theexcessmucuscausesmucousplugs,trapping carbondioxide,increasingPaCO2,anddecreasingPaO2,resultinginanincreasedriskofinfectionand corpulmonale.
49. What is bronchiectasis?
Bronchiectasisisaconditioninwhichthebronchiareabnormallyandirreversiblydilateddueto
destructionofthemuscleandelasticityofthelungparenchymasecondarytoinammation.The disordercanbeassociatedwithcongenitallungdiseasesortheresultofavarietyofpulmonary insultsincludingaspirationorsevereinfection.Theresultantdilationanddestructioncausesthelung toinadequatelyclearsecretionsandbecomecolonizedwithpathogenicbacteria,resultinginrecurrent pulmonaryinfections.
50. What is adult respiratory distress syndrome (ARDS)?
ARDSisaC5a-inducedneutrophilaggregationinthelung.Thisaggregationisoneofthemajor
mechanismsofpathologyofARDS.Thedamagedcapillariesleakprotein-richuidintotheintersti­tium,whichleadstochangesinpulmonaryfunction.
51. What causes ARDS?
ARDSusuallyresultsfromaninjurytothealveolar-capillarymembrane.Italsocanbecausedby
anexistingunderlyingdisease,suchassystemicsepsis,fatembolism,headinjury,aspiration, pancreatitis,orinhalationinjury.Patientstypicallyshowseveredyspneaandhypoxemiarefractoryto supplementalO2withdiffusepulmonaryinltratesonchestradiograph.
52. What is the appropriate management of ARDS?
ManagementofARDSincludesimmediatetransfertoanintensivecareunitandplacementofa
pulmonaryarterycatheterwithmechanicalventilationtomaintainthepulseoximetry(SpO2)>90%, whichcorrespondstoPO2>60mmHg.Inaddition,thepulmonarycapillarypressureshouldbekeptin therangeof12to15mmHg,andthecardiacindexshouldbemaintainedabove3L/min/m2.Treat­mentofARDSisgenerallysupportivetoachieveO2saturationof90%whileminimizingbarotrauma andoxygentoxicity.
53. What are the features of ARDS?
• Historyofmajorinsult  • Increasedrespiratorydistress  • DiffuseinltrationonchestX-ray  • Hypoxemia(PaO2<60mmHgwithFiO2>0.6)  • Respiratoryalkalosis  • Normalpulmonarycapillarywedgepressure(PCWP)  • Decreasedpulmonarycompliance  • Increasedshuntfunction  • Increaseddeadspaceandventilation
54. How often does aspiration occur, and what are the complications?
Aspirationisarelativelyrareoccurrenceaffectingapproximately1outofevery10,000patients
undergoinggeneralanesthesia.Intheoutpatientsetting,deepsedationwithoutasecureairwayhas alsobeenshowntobesafewithoutasignicantincreasedriskforaspiration.Complicationsinclude bronchospasm,pneumonitis,pneumonia,acuterespiratorydistresssyndrome,lungabscess,and empyemaconferringanincreasedriskofmortality.
55. What are common risk factors for aspiration?
• InadequateNPOstatus(emergentcases)orfailuretofollowNPOguidelinesforanesthesia  • Extremesofage(twiceascommoninchildrenandelderly)  • Medicationsthatdecreaselevelofconsciousness(sedative/hypnotics/anxiolytics)andbluntprotec-
tivereexes  • Headtrauma  • Stroke
190 PART IV MANAGEMENTCONSIDERATIONS
https://t.me/medicina_free
• Presenceofanasogastrictube  • Prolongedsupineposition
56. What is the appropriate management of aspiration?
Abaselinechestradiographshouldbeobtainedforanypatientsuspectedofaspiration.Afterimme-
diatesuctioning,supportivecareisthemainstayoftreatmentandincludessupplementaloxygen andmonitoringofoxygensaturationinaninpatientsetting.Ventilatorysupportshouldbeinitiated ifconcernforrespiratoryfailurearises(seequestion12above).Antibioticsshouldnotbeinitiated unlesstheeventleadstopneumoniaandculturescanbetailoredtotargetspecicorganisms. Classically,aspiratedmaterialconsistsofgram-negativeoranaerobicorganisms(oral/gastroin­testinalora).Aspirationofgastriccontentscanleadtochemicalpneumonitisandalsorequires supportivecare.
57. How can aspiration risk be decreased?
Byrecognizingsurgicalpatientswhoarehighrisk,adjunctivestepsandmedicationcanbetakento
minimizetheoverallrisk.Adheringtostandardfastingprotocolspriortoanyprocedurewilloptimize gastricemptying.Gastricacidscanbeneutralizedwithantacidsorhistaminereceptorantagonists. Logically,pro-motilityagentssuchasmetoclopramidewillaidingastricemptying;however,nodata supportsthis.Aspirationcanbepreventedincriticallyillpatientsbymaintainingthehead-of-bed 30degrees,minimizingsedatives,andavoidingbolusfeedsinhigh-riskpatients.
58. What drugs interfere (interact) with aminophylline?
Themostcommonlyciteddrugiserythromycin,whichincreasesserumlevelsofaminophylline.
Cimetidinealsoincreasesserumlevelsofaminophylline.
59. What are the signs and symptoms of pulmonary embolism (PE)?
PEcanpresentwithacuteonsetofpleuriticchestpain,dyspnea,syncope,orlegpainandswelling.
Manypatientsmayhavenosymptoms.SignsofaPEincludetachypnea,hypoxemia,rales,unex­plainedtachycardia,elevatedjugularvenouspressure,andlow-gradefever.RiskfactorsforPEinclude stasis(immobility,obesity),recentendothelialinjury(trauma,surgery,recentfracture,anddeepvein thrombosis),andhypercoagulablestate(pregnancy,oralcontraceptiveuse,malignancy).
60. How is the pre-test probability of deep vein thrombosis (DVT) determined?
TheWell’scriteriaisamethodofdeterminingthelikelihoodofDVT.Itisbasedonmajorandminor
criteria.Majorcriteriaincludeactivecancer,immobilization,bedrest>3days,majorsurgerywithin 4weeks,swellingofthethighandcalf,familyhistoryofDVT.Minorcriteriaincluderecenttraumato symptomaticextremitywithin60days,pittingedema,dilatedsupercialveins,erythema,andrecent hospitalizationwithin6months.Ifmorethanthreemajorcriteriaortwomajorandtwominorcriteria aremet,thenthereisahighlikelihoodthatDVT/PEcanbepresent(85%+DVT).
61. How is PE diagnosed?
ImmediateABG,electrocardiogram(ECG),andchestX-rayshouldbeobtained.TheABGwill
revealhypoxemia,hypocapnia,andrespiratoryalkalosiswithanincreasedA–agradient.AnECG mayrevealsinustachycardiaoratrialbrillationwithsignsofrightventricularstrain(e.g.,right bundlebranchblockwitht-waveinversionsinleadsV1-V4).ChestX-raymayshowatelectasis, effusion,andaraiseddiaphragm.WithalargePE,thechestX-raymayhaveaHamptom’shump,a wedge-shapeddensityabuttingthepleura,orWestermarksign,whichsharplycutsoffofavessel distaltotheembolus.D-dimerlevelscanbeassessedwithhighsensitivitybutpoorspecicity.If thepatientisexperiencinganyasymmetricswellinginanyextremity,thenDVTshouldberuled outwithanultrasound.BypassingtheselaboratorytestsandobtainingCTangiographymaybe warranted.
62. What is the appropriate management of postoperative PE?
Oncethepatienthasbeenstabilized,treatmentincludesacuteanticoagulationwithintravenousor
subcutaneousheparinoralowmolecularweightheparin.Ifgivenintravenously,heparinshouldbe titratedtoagoalPTTof60to85seconds.Oncesuitableacuteanticoagulationhasoccurredand PTTistherapeutic,thepatientistransitionedtoanticoagulationwithwarfarin(goalINRof2to3for 3to6monthspostevent).Withacontraindicationforanticoagulation,aninferiorvenacavalter shouldbeplaced.ForlargeproximalPEwithhemodynamiccompromise,thrombectomymaybe considered.
CHAPTER 17 RESPIRATORYDISORDERS 191
https://t.me/medicina_free
BiBliography
BarashP,CullenB,StoeltingR,etal.:Clinical anesthesia,ed2,Philadelphia,1996,Lippincott-Raven. BatesB,BickleyL,HoekelmanR:Thethoraxandlungs.InBatesB,editor:A guide to physical examination and history
taking,ed6,Philadelphia,1995,J.B.Lippincott.
BradleyTD,RutherfordR,GrossmanRF,etal.:Roleofdaytimehypoxemiainthepathogenesisofrightheartfailureinthe
obstructivesleepapneasyndrome,Am Rev Respir Dis131:835,1985.
ChungF,YangY,LiaoP:PredictiveperformanceoftheSTOP-Bangscoreforidentifyingobstructivesleepapneainobese
patients,Obes Surg23(12):2050–2057,December2013.
CohenMM,DuncanPG,PopeWD,WolkensteinC:Asurveyof112,000anaestheticsatoneteachinghospital(1975–83),
Can Anaesth Soc J33:22–31,1986.
DeanG,JacobsAR,GoldsteinRC,GevirtzCM,PaulME:Thesafetyofdeepsedationwithoutintubationforabortioninthe
outpatientsetting,J Clin Anes23:437–442,2011.
GottliebDJ,YenokyanG,NewmanAB,etal.:Prospectivestudyofobstructivesleepapneaandincidentcoronaryheart
diseaseandheartfailure:thesleephearthealthstudy,Circulation122:352,2010.
KearneyDJ,LeeTH,ReillyJJ,etal.:Assessmentofoperativeriskinpatientsundergoinglungresection,importanceof
predictedpulmonaryfunction,Chest105:753–759,1994.
KispertJF,KazmersA,RoimanL:Preoperativespiromterypredictspredictsperioperativepulmonarycomplicationsafter
majorvascularsurgery,Ann Surg58:491–495,1992.
KollefM,GoodenbergerD:Criticalcareandmedicalemergencies.InEwaldG,McKenzieC,editors:The Washington manual
of medical therapeutics,Boston,1995,Little,Brown.
LiKK:MaxillomandibularAdvancementforobstructivesleepapnea,J Oral Maxillofac Surg69(3):687–694,March2011.
EpubDecember24,2010.
Martínez-GarcíaMA,Campos-RodríguezF,Catalán-SerraP,etal.:Cardiovascularmortalityinobstructivesleepapnea
intheelderly:roleoflong-termcontinuouspositiveairwaypressuretreatment:aprospectiveobservationalstudy, Am J Respir Crit Care Med186:909,2012.
MillerR,StoeltingR:Acid-baseandbloodgasanalysis.InMillerR,editor:Basics of anesthesia,ed3,NewYork,1994,
ChurchillLivingstone.
MillerWP:Cardiacarrhythmiasandconductiondisturbancesinthesleepapneasyndrome.Prevalenceandsignicance,
Am J Med73:317,1982.
MurrayMJ,CoursinDB,PearlRG,ProughDS:Critical care medicine perioperative management,ed2,Philadelphia,2002,
Lippincott.
NationalAsthmaEducationandPreventionProgram:Expert panel report III: guidelines for the diagnosis and management
of asthma,Bethesda,MD,2007,NationalHeart,Lung,andBloodInstitute(NIHpublicationno.08-4051).
www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm.
OlssonGL,HallenB,Hambraeus-JonzonK:Aspirationduringanaesthesia:acomputer-aidedstudyof185,358anaesthet-
ics,Acta Anaesthesiol Scand30:84–92,1986.
PettitTW,CobbJP:Criticalcare.InDohertyGM,WellsSA,BaumannDS,etal.:The Washington manual of surgery,Boston,
1997,Little,Brown.
PunjabiNM,CaffoBS,GoodwinJL,etal.:Sleep-disorderedbreathingandmortality:aprospectivecohortstudy,PLoS Med
6:e1000132,2009.
RoserSM:Managementofthemedicallycompromisedpatient.InKwonP,LaskinD,editors:Clinician’s manual of oral and
maxillofacial surgery,ed2,Chicago,1997,Quintessence.
VanaKD,SilvaGE,GoldbergR:PredictiveabilitiesoftheSTOP-BangandEpworthSleepinessScaleiniden-
tifyingsleepclinicpatientsathighriskforobstructivesleepapnea,Res Nurs Health36:84–94,2013,
http://dx.doi.org/10.1002/nur.21512.
WellsPS,etal.:Derivationofasimpleclinicalmodeltocategorizepatientswithaprobabilityofpulmonaryembolism:
increasingthemodelsutilitywiththeSimpliREDD-dimer,Thromb Haemost83(3):416–420,2000.
WellsPS,etal.:Excludingpulmonaryembolismatthebedsidewithoutdiagnosticimaging:managementofpatientswith
suspectedpulmonaryembolismpresentingtotheemergencydepartmentbyusingasimpleclinicalmodelandd-dimer,
Ann Intern Med135(2):98–107,2001. WestJB:Respiratory physiology: the essentials,ed9,Baltimore,2012,Lippincott,Williams,andWilkins. WestJB:Pulmonary pathophysiology: the essentials,ed8,Baltimore,2012,Lippincott,Williams,andWilkins. YoungT,FinnL,PeppardPE,etal.:Sleepdisorderedbreathingandmortality:eighteen-yearfollow-upoftheWisconsin
sleepcohort,Sleep31:1071,2008.