Presentation Chapter 27 Pulmonary Embolism and ARDS Case

7/21/2019 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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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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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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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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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

Presentation Chapter 27 Pulmonary Embolism and ARDS Case

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