Presentation Chapter 27 Pulmonary Embolism and ARDS Case
Transcript of Presentation Chapter 27 Pulmonary Embolism and ARDS Case
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Chapter 27Pulmonary embolism
(the most under-diagnosed cause of death)
Ross Klingsberg, M
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Clinical !ignette "
# $2-year-old %oman under%entbilateral &nee replacement and %asdischarged %ithout complications on
postoperati'e day t%o ine days aftersurgery she de'elops se'ere respiratorydistress and dies suddenly in theemergency department Postmorteme*amination of her pulmonary arteryre'eals the pathology seen in the image+
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hat medical condition could predispose to asimilar pathology as obser'ed in this patient
# #spiration
. /actor !de0ciency
C /actor !111de0ciency
Protein Cde0ciency
3hrombocytopenia
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Clinical !ignette 2
# $4-year-old obese man presented tothe emergency department %ithlightheadedness progressing to near-
syncope and progressi'e shortness ofbreath of three days5 duration
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6is symptoms started a %ee& ago%hen he 0rst e*periences pleuriticchest pain that radiated to his right
side
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6e had undergone sinus surgery %ee&sprior to presentation
6is past medical history %as signi0cant for
hypertension, obstructi'e sleep apnea, anddiastolic heart failure
# deep 'ein thrombosis (!3) follo%ing&nee surgery had occurred "8 years
pre'iously
6e 9uit smo&ing 2: years ago and did notreport alcohol use
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Physical e*am re'ealed tachypnea,sinus tachycardia at a 6R ; ""4beats
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i'en the high clinical suspicion foracute P, a C3 angiogram of thechest %as performed that re'ealed
multiple 0lling defects
3he patient %as thereafteranticoagulated %ith lo%-molecular
%eight heparin (@M6)
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@earning obDecti'es
escribe the clinical symptoms and sign ofpatients presenting %ith pulmonary embolism
e0ne the pathophysiology of P and the ris&
strati0cation of patients diagnosed %iththromboembolism
'aluate shoc& and right 'entricular dysfunctionas a discriminator of outcome during or after P
Pro'ide a step%ise approach to the treatment ofpatients diagnosed %ith acute P
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1mportant points toremember
Pulmonary embolism (P)
!enous 3hrombo-mbolism (!3)
eep !ein thrombosis (!3)
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Pathophysiology
!
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1mportant points
iagnosis and therapy reducesmorbidity
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Euestions for discussion
hat materials can become embolito the lungs
hat are the physiological e'entsthat predispose to the de'elopmentof !3
hat are e*amples of strong,
moderate, and %ea& ris& factors for!3
hat are the hereditary ris& factors
for !3
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onthrombotic pulmonaryemboli
/at embolism
2G-G4 hour delay
yspnea, petechiae and mental confusion
#mniotic Fuid embolism #ir embolism
3rendelenbergchistosomiasis >eptic emboli
Ather emboli
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Ris& factors for 'enous
thromboembolism
>trong 6ip, pel'is, or leg fracture
Knee or hip replacement surgery
MaDor trauma
>pinal cord inDury
#ntiphospholipid antibody syndrome (#P@#>)
Moderate
Prior !3 Postpartum period
Malignancy
strogen therapy, oral contracepti'es
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ea& ris& factors for 'enous
thromboembolism
#d'anced age H$: years
Abesity
#ntipartum period !aricose 'eins
>tro&e
Respiratory failure 1nd%elling central 'enous catheter
#rthroscopic &nee surgery
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6ereditary ris& factors for 'enous
thromboembolism
/actor ! @eiden mutation
Protein C or > de0ciency
6yperhomocysteinemia Prothrombin gene mutation 2:2":#
#ntithrombin 111 de0ciency
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Clinical presentation
Pre'alence
Causes ":? of all in-hospital deaths
.iggest cause of maternal deaths associated
%ith li'e births ":7? probability by age 4:
Most fatal P are unrecogniBed and undiagnosed
ecision rules (ell5s criteria) help in the
diagnostic process P cannot be ruled in or out by history and
physical
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#cute pulmonary embolism
symptoms
SymptomAll patients(N=383)(%)
No previouscardiopulmonarydisease (N=117)(%)
yspnea 74 7
Pleuritic chest pain 8= $$
Cough G 7
@eg Pain 27 2$
6emoptysis "$ "Palpitations " ":
heeBing "G =
#ngina-li&e pain $ G
P1AP "==:
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iIerential diagnosis
Pneumonia Pneumothora* Pleural eIusion
Pulmonary edema #sthma e*acerbation CAP e*acerbation
Myocardial infarction Congesti'e heartfailure
#cute pericarditis
sophagealdysmotility
astroesophagealreFu* disease
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Pre-test probability of P(ells criteria)
Clinical characteristic Score
#cti'e cancer (treatment %ithin $ months orpalliati'e
"
>urgery or bedridden for J days for past G %ee&s "8
6istory of deep 'enous thrombosis or pulmonaryembolism "8
6emoptysis "
6eart rate H":: beats et al 2:::
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-dimer
Cross-lin&ed 0brin deri'ati'e
H8:: mcg
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Cardiac biomar&ers
Cardiac troponin 3 and troponin 1both ele'ated in acute P
.P may be ele'ated (eg ::-7::)in acute P (caution+ do notmisdiagnose C6/)
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#rterial blood gas analysis
6ypo*emia
P1AP+ #-a diIerence increased bymore than 2: in 7$ of 44 (4$?)
pCA2usually lo%, but high pCA2does
not rule out P
#-a diIerence may be normal inother%ise healthy persons
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Chest radiograph
P1AP+ abnormal in =4 of ""7 (4G?) #telectasis andymptoms O no bronchospasm, no e'idence of
anatomical cardiac shunt, and normal CRsuggest P
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lectrocardiography
P1AP+ GG of 4= patients (G=?)
3-%a'e changes, >3-segmentabnormalities, left or right a*isde'iation
>"E3 pattern, R..., P-%a'epulmonale, right a*is de'iation
occurred in 2$?
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!entilation-perfusion (!
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>piral (helical) C3 scanangiography
Re9uires contrast bolus
P1AP 11 sho%ed C3 preferred o'er!
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>piral C3 for diagnosis ofacute PAdvanta$es
#'ailability
>ensiti'ity and
speci0city for centralemboli
Relati'e rapidity
iagnosis of other
conditions Multiplanar
reformation
>afety
imitations
1! contrast re9uired
Reader e*pertise
re9uired ot portable
Morbid obesity maypre'ent
Relati'econtraindications Renal insuciency
Contrast allergy
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chocardiography
May suggest P
Clot may be directly obser'ed
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3reatment
#cute P Qnfractionated heparin
@o%-molecular %eight heparin
3hrombolytics
1nferior 'ena ca'a 0lters
Chronic P arfarin >urgical
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Qnfractionated heparin(Q/6)
4: units
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6eparin-induced thrombocytopenia
(613)
8? incidence %ith Q/6
:$? incidence %ith @M6
8:? reduction in platelets after 8days or absolute reduction of"::,::: per mm 1f present, then treat %ith argatroban or
hirudin
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3hrombolytics
>trepto&inase
Qro&inase
Recombinant tissue plasminogen acti'ator
(rt-P#) Qsually used in P %ith shoc&
'idence for use %ith large P %ithout shoc&
2? ris& of intracranial hemorrhage
Mechanical thrombectomy sometimesperformed
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!ena ca'a interruption (1!C0lter)
hen anticoagulation is contraindicated
hen @ clot burden is large
hen bleeding occurs on anticoagulation
Remo'able 0lters are no'el
Ris&s insertion-related complications
0lter migration direct thrombus e*tension through the 0lter
1!C thrombosis
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>urgical thrombectomy
Qsually for chronic P
May be considered for acute P %henanticoagulation is problematic
.eing replaced by inter'entionalradiology mechanical thrombectomy
Anly performed a specialiBed centers
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Case studies
# 8=-year-old man undergoes total &neereplacement for se'ere degenerati'e Dointdisease 3%o days after surgery, he
de'elops acute onset shortness of breathand right-sided pleuritic chest pain 6e isno% in moderate respiratory distress %itha respiratory f ; 24 breaths
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6is lung e*am is normal and his cardiace*am re'eals sinus tachycardia but isother%ise unremar&able
3he right lo%er e*tremity is postsurgical,healing %ell, %ith 2O pitting edema, calftenderness, erythema, and %armth
3he left leg is normal @aboratory %or&up re'eals a serum
creatinine of "$ mg
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hat is the most appropriate ne*tdiagnostic step
# !
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# 82-year-old obese %oman %ho isreco'ering from a 'iral illness presents%ith acute onset shortness of breath of
hours duration >he rpoet symptomsof ocugh and is 'ery an*ious as shenoticed blood in her sputum,
appro*imately "-2 teasopoonfuls in9uantity #t the time of presentationher initial .P ; =:
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6er C re'eals sinus rhythm %ithnormal PR and ER> inter'als, ho%e'erthe medical student points out the >",
E111, and 3111 pattern # helical C3 scan%ith a P protocol is obtained %ith0ndings of bilateral 0lling defects in
the interlobar pulmonary arteries
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hich of the follo%ing is the most appropriatene*t treatment for this patient
# #rrange for 1!C 0lterplacement
. .egin %arfarin therapy
C 1nitiate unfractionated
heparin to achie'e atherapeutic aP33
Abtain a pulmonaryangiogram to con0rm a
diagnosis of P Place a central 'enousline and begin
thrombolytic therapy
>uspicion ofP
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P>table 1CQpatients
>tartanticoagulation if
no contraindications
>piral C3or !3AP aftera negati'e spiral C3 or
lo%-prob !
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pQnstable 1CQ
patients
>tart anticoagulation if nocontraindications
Q of legs and upperbody if C!C
Continue anticoagulation chocardiogram
R! dilation, dysfunction,or clot
Considerthromboly
sis
ormal R!
Consider bedside angiographyor perfusion scan
Continueanticoagulation >top anticoagulation
&
& '
'
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AC#" N *N+,- AN. #/" AC#","SP*,A#0,- .*S#,"SS S-N.,0"
Chapter 24
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Key concepts
#R> 's #@1
Cardiogenic 's non-cardiacpulmonary edema
@ung protecti'e strategy
PP
#l'eolar recruitment
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#R> Problem-based @earning CasePresentation
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@earning obDecti'es
>tudents %ill be able to+ Correctly diagnose #R> using the consensus
de0nition of the syndrome and diIerentiate it from'olume o'erload and cardiogenic pulmonary edema
e0ne, list, and e*plain the pathophysiologicale'ents during the acute proliferati'e and the0brosing-al'eolitis stages of #R>
e0ne and e*plain the physiologic rationale of PPand the haBards of using positi'e pressure 'entilation
Perform a basic interpretation of an arterial blood gas
*plain the eIect of increased intrathoracic pressureon left 'entricular 0lling (preload) and blood pressure
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Rele'ant terms
#R> S acute (adult) respiratory distress syndrome (a&a,shoc& lung, non-cardiogenic pulmonary edema)
#. S arterial blood gas
pCA2S partial pressure of carbon dio*ide in blood
pA2S partial pressure of o*ygen in blood
Ppea&S pea& air%ay pressure (on 'entilator)
PplatS plateau air%ay pressure (on 'entilator)
!
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Case presentation
# 8-year-old pre'iously healthy%oman is brought to the R %ith aclose-range gunshot %ound to the
abdomen 3hirty minutes afterarri'ing, her blood pressure is G:
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Case (continued)
>he 9uic&ly recei'es "8 liters ofcolloid and 2 liters of normal saline6er blood pressure rises to 4:
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Case (continued)
@ater in the day, her breathing becomesmore dicult and labored >he is breathingrapid shallo% breaths at G: per minute #n
arterial blood gas at that time sho%s p6 of 7G
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Euestion for discussion
>ince she is breathing rapidly(hyper'entilating) and her pCA2is : mm
6g (normal 8-G8) %hy is the p6 7G
e %ould e*pect al&alemia, %ith p6 H7G:, dueto the lo% pCA2
ormal p6 is probably due to an underlyingmetabolic acidosis, %ith respiratory
compensation 1n the setting of hemorrhagic shoc&, the most
li&ely type of metabolic acidosis is lactic acidosis
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6ospital course (continued)
8:? :2(/iA2 :8) is administered by a
'enturi face mas&, and the pA2 rises to $:mm 6g
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Physical *amination
en+ %ell-oriented, but ill-appearing
Chest+ anterior and posteriorcrac&les, %ithout rubs, and no
dullness to percussion
6eart+ no displacement of PM1, nogallops, rubs, or murmurs, normal
N! #bd+ post-surgical
*t+ diIusely decreased deep-tendon
reFe*es
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#rterial blood gas
3he ne*t day, on 8:? o*ygen, her#. sho%s+
p6, 7G4
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Clinical course (continued)
#.
p6, 7G$
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Course (continued)
>he is intubated and mechanical'entilation is initiated3idal 'olume, $:: ml
Rate, 2: breaths per minute /1A2,": ("::? o*ygen)
Pea& air%ay pressure is recorded at G4 cm62A (normal is :)
#.
p6 78
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/indings
chocardiogram+ normal right and left'entricular function
3idal 'olume (!t) decreased to 8: m@
based upon her predicted body %eightof 8= &g
#.
p6 7, pCA2$8, and pA28 mm6g Pea& inspiratory pressure decreased to
2$ cm62A
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Euestions for discussion
hat is the diagnosis for her respiratorycondition
#cute respiratory distress syndrome (#R>)
hat are the criteria to ma&e this diagnosis" #cute onset respiratory failure (less than 7
days) after a precipitating e'ent
2 .ilateral pulmonary opacities
PaA2
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hat pathophysiological abnormalities are found in#R>
T>tiIU (non-compliant) lungs are harder to inFate
amaged al'eoli 0lled %ith proteinaceous Fuid,cellular debris, and hyaline membranes, %hichlo%ers the !
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Iect of positi'e pressureon /RC
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Euestions for discussion
hy does the patient ha'e #R> and notcardiogenic pulmonary edema
3he echocardiogram %as normalL no e'idenceof congesti'e heart failure
# diagnosis of #R> implies no clinicale'idence of ele'ated left atrial pressure, or a
pulmonary capillary pressure "4 mm6g
Pulmonary edema usually begins %hen pulmonarycapillary pressure is H 2" mm6g assuming normaloncotic pressure and integrity of lung capillaries
3he Tsafety factorsU that pre'ent
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3he safety factors that pre'ental'eolar (airspace) Fooding
V ilutional interstitialoncotic pressure
W Peri'ascular cungX Remo'al through
lymphatics
3hus, it ta&es about 2"mm6g or greater ofpulmonary capillarypressure for healthyadults to de'elopairspace edema
#l'eolar edema occurs%hen interstitial'olume increases byabout G:?
#nnals of 1nternal Medicine, 2" >eptember 2::G !ol "G" ($) pp G$:-G7:
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6ospital Course
1n spite of this therapy, forty-eighthours later, the pA2had again fallen
to G4 mm6g %hile breathing "::?
A2(/iA2 ":) .ecause of this, thepositi'e end-e*piratory pressure(PP) %as increased to "2 cm 62A
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Euestions
hy didn5t "::? o*ygen raise her arterial pA2more Right to left shunting of blood through Fooded al'eoli
Can you gi'e an estimate of her lung compliance %iththe tidal 'olume 8: m@ and inspiratory pressure
(plateau pressure S PP) "$ cm 62A Compliance ; Y 'olume
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>ingle mechanically 'entilated
al'eolus
Pressures during mechanical 'entilation
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Pressures during mechanical 'entilation
Pea& pressure (Ppea&) Plateau
pressure (Pplat)
Ppeak Pplat; air%ay Fo% resistance
Marino 2nded
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6ospital course (continued)
1ncreasing the PP raised her pA2to
7: mm6g #t this point her pea&inspiratory pressure (Ppea&) %as 2
cm62A and plateau pressure (Pplat)
%as 24 cm62A 6er blood pressure
fell to 4:
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preload (particularly in the presence of decreased intra'ascular 'olumestatus)
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6ospital course (continued)
hat is the ne*t step to address herlo% blood pressure
i'e 1! Fuids
# 8:: m@ bolus of :=? salinesolution raised her blood pressure to
=8
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Euestion
hat does PP do PP reopens al'eoli that are collapsed
but still can be recruited %ith positi'e
air%ay pressure PP &eeps the collapsing al'eoli from
continuous opening and closing %ith eachrespiratory cycle
PP &eeps the respiratory cycle on themost fa'orable portion of the'olume
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#mato et al #NRCCM"==8
Compliance ; Y 'ol
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!a al'eoli onthe left diagram lo%er than blood Fo% to the #R> al'eolion the right diagram 3he Fooded al'eoli causes hypo2ic pulmonary
Z
hat is the ris& of e*cessi'ely high air%ay
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hat is the ris& of e*cessi'ely high air%aypressures
.arotrauma from o'er-distention and damage tohealthy al'eoli
Capillary lea& from pressure-damaged al'eoli
ecreased 'enous return (preload) to the left
'entricle 1f local al'eolarpressure e*ceeds capillary
pressure, then blood redistributesto lesscompliant damaged areas and %orsens gase*change
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3he goal of positi'e pressure 'entilation is torecruit collapsed al'eoli %ithout o'erstretching the
healthy al'eoli Marini-heeler 2nded
1ncreased air%ay pressure 'iamechanical 'entilation
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/aard o!positive
pressuremechanicalventilationM! * 4 %ee&s,Ppea&8:-7:
mm6g/iA2 4:-"::?
4** ' !entilator-induced lung
6 it l ( t5d)
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6ospital course (cont5d)
3he patient subse9uently impro'ed #fterse'eral days of mechanical 'entilation, herpA2rose and her chest radiograph sho%ed
some clearing 3he /iA2needed to maintain a
pA2greater than $: mm 6g on #. and >pA2
on pulse o*imetry to greater than =2?decreased to :8
hat are the e'ents that led to clearing ofher lungs and impro'ed respiratory status
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Mechanisms in the resolution of
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Mechanisms in the resolution of
#R>
Proliferation and diIerentiation of al'eolartype 11 pneumocytes
Resorption of al'eolar edema 'ia energy
dependent sodium pumps on type 11pneumocytes and mo'ement of %aterthrough a9uaporins on type 1 pneumocytes
Remo'al of cellular debris by al'eolar
macrophages radual remodeling and resolution of
intraal'eolar and interstitial granulationtissue and 0brosis
/ ll ti
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/ollo%-up 9uestions
hat caused the damage to her lungsafter her initial surgery @i&ely shoc&, multiple transfusions and
probable sepsis amage to the lungs can be direct (ie
pneumonia, aspiration of gastric content) orindirect (ie sepsis, se'eretrauma
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/ollo%-up 9uestions
hat physiologic changes caused her tohyper'entilate after surgery 6ypo*emia
>epsis
Can cause lactic acidosis (%hen se'ere) andhyper'entilation (e'en to the point ofo'ercompensation and induction of respiratoryal&alosis)
1ncreased dead space+tidal 'olume ratio ma&esthe lungs inecient at remo'ing CA2
1ncreased areas of lo% !
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/ollo%-up 9uestions
Can shunt be o'ercome %ith increased /iA2 o, shunt cannot be o'ercome by increased o*ygen administration
because there is no al'eolar 'entilation
hat determines pCA2
3he rate of CA2remo'al from the blood is determined by al'eolar
'entilation
hy is rapid shallo% breathing less ecient than slo% deepbreathing
1ncreased dead space+tidal 'olume ratio increase the amount of'entilation re9uired to &eep pCA2constant
hy %ould o*ygen re9uirement increase in a situation of poorlung compliance li&e #R>
3he %or& of breathing is increased due increased dead space+tidal'olume ratio and increased eIort to e*pand the lungs
/ ll ti
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/ollo%-up 9uestions
oes hydrostatic pressure play a role in%orsening of the al'eolar 0lling process in#R> Ancotic pressure
[es, hydrostatic pressure can play animportant role, especially if there aredamaged, Tlea&yU capillaries
Ancotic pressure also plays a role, especially
%hen coe*isting health problems e*ist li&emalnutrition, nephrotic syndrome, and
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yin #R> (e'en more so if serumalbumin is lo%)
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3he end
Coming ne*t+Chapter 24, Pathophysiology and iseasesof the Pleural >pace,
Chapter 2=, Principles and oals ofMechanical !entilation