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PneumologieDCEM4QCM

DrBenjaminPlanque6e

Ansdegrâce2015-2016

Ques-on

A. Scin-graphiedeven-la-on-perfusionB. EchographiecardiaqueC. EchographiedesmembresinférieursD. AngioscannerthoraciqueE. DDimères

Réponse

A. Scin-graphiedeven-la-on-perfusionB. EchographiecardiaqueC. EchographiedesmembresinférieursD. AngioscannerthoraciqueE. DDimères

Ques-on

A. FréquencerespiratoireB. PressionartérielleC. Agedupa-entD. Unantécédentd'EPE. Ladilata-ondescavitésdroitessur

l'angioscanner

Réponse

A. FréquencerespiratoireB. PressionartérielleC. Agedupa-entD. Unantécédentd'EPE. Ladilata-ondescavitésdroitessur

l'angioscanner thatRVischaemiais ofpathophysiologicalsignificance intheac ute phaseofPE. 76-78

AlthoughRV infarctionisuncommonafter PE,it

islikelythat theimbalancebetw eenoxygen supplyanddemand can resultindamagetocardiomy ocytesand furtherreduce contractile forces. circulationaresummarizedinFigure1. RespiratoryfailureinPEis predominantly aconsequenceof haemodynamicdisturbances. 79

Lowcardiacoutputresults indesat-

urationofthemixedveno usblood. Inaddition,zones ofreduced flowinobstructedves sels,combinedwith zonesofoverflowin the capillarybedserved bynon-obstructed vessels,res ultinv entila- tion-perfusionmismatch,whichcontributesto hypoxaemia.In aboutone-thirdof patients,right-to-leftshunting through apatent foramenovalecanbedetected byechocardiography: thisiscaused byaninverted pressuregrad ientbetween therightatriumandleft atriumandmayleadto severehypoxaemia andanincr easedriskof paradoxicalembolizationandstr oke. 80

Finally,eveniftheydo not

larhaemorrhageres ultinginhaemopty sis,pleuritis,andpleuraleffu- sion,whichis usuallymild.This clinicalpresenta tionisknown as 'pulmonaryinfarction'.Its effectongas exchangeis normallymild, exceptinpatientswithpre-e xistingcardior espirat orydisease.

2.5Clinicalclassific ationof pulmonary

embolismseverity Theclinicalclassifica tionofthe severityofanepisode ofacute PEis basedonthe estimatedPE-rela tedearly mortalityriskdefinedby in-hospitalor30-day mortality(Figure2).Thisstr atification, which hasimportantimplications bothforthe diagnostic andtherapeutic icalstatus atpresentation,withhigh-riskPEbeingsuspected orcon- firmedinthe presenceof shockor persistentarterialhypotension andnothigh-riskPEintheir absence.

3.Diagnosis

ment,'confirmedPE' isdefinedas aproba bilityofPE highenoughto indicatetheneedforPE-specific treatment,and 'excludedPE' asa probabilityofPElowenough tojustifywithholdingPE-specific treat- mentwithan acceptablylo wrisk.

3.1Clinicalpr esentation

arenon-specific( Table3).Whenthe clinicalpresentation raises the suspicionofPE inanindividual patient,it shouldprompt further objectivetesting.Inmostpat ients,PEissuspectedo ntheba sisofdys - pnoea,chestpain,pr e-syncopeorsync ope,and/orhaemo ptysis. 81-83
Arterialhypotensionand shockare rarebut importantclinicalpr e- sentations,sincetheyindicatecentral PEand/or aseverely reduced lessofthe presenceof haemodynamicinstability . 84

Finally,PEma y

becompletelyasym ptomaticand bediscoveredincidentallyduring diagnosticwork-upfor anotherdisease oratautopsy . Chestpainis afrequent symptom ofPEand isusuallycausedby 85
Incentral PE,chestpainmayhave atypicalanginacharacter,possibly coronarysyndrome (ACS)oraorticdissection.Dyspno eamaybe acuteandsev ereincentral PE;insmallperipheral PE,itis often mildandma ybetransien t.Inpatientswithpre-existing heartfailure orpulmonarydisease, worseningdyspnoea maybe theonly symptomindicative ofPE.

Increased RV afterload

RV O 2 delivery

TV insufficiency

RV wall tension

Neurohormonal

activation

Myocardial

inflammation RV O 2 demand

RV ischaemia

RV coronary

perfusion

RV outputRV contractility

Systemic BP

Cardiogenic

shock Death

RV dilatation

Low CO

LV pre-load

BP = blood pressure; CO = cardiac output; LV = left ventricular; RV = right ventricular; TV = tricuspid valve. Figure1Keyfactorscontributing tohaemodynamiccollapse in acutepulmonaryembolism

Suspected acute PE

Shock or hypotension

a YesNo

High-risk

b

Not high-risk

b

PE = pulmonary embolism.

a by !40 mm Hg, for >15 minutes, if not caused by new-onset arrhythmia, hypovolaemia, or sepsis. b Based on the estimated PE-related in-hospital or 30-day mortality.

Figure2Initialrisks tratification ofacutePE.

ESCGuidelinesPage7of 48

by guest on August 30, 2014 http://eurheartj.oxfordjournals.org/

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Ques-on

A. FréquencedessymptômesdiurnesB. FréquencedessymptômesnocturnesC. ValeurduDEPD. ValeurduVEMSE. Limita-ond'uneac-vitéphysique

Réponse

A. FréquencedessymptômesdiurnesB. FréquencedessymptômesnocturnesC. ValeurduDEPD. ValeurduVEMSE. Limita-ond'uneac-vitéphysique

GINA/CEP2015

HOW TO ASSESS ASTHMA CONTROL

Asthma control means the extent to which the effects of asthma can be seen in the patient, or have been reduced or removed by treatment. Asthma control has two domains: symptom control (previously called 'current clinical control') and risk factors for future poor outcomes. Poor symptom control is a burden to patients and a risk factor for flare-ups. Risk factors are factors that increase the patient's future risk of having exacerbations (flare-ups), loss of lung function, or medication side-effects. Box 4. Assessment of symptom control and future risk

A. Level of asthma symptom control

In the past 4 weeks, has the patient had:

Well controlled

Partly

controlled

Uncontrolled

Daytime symptoms more than twice/week? Yesquotesdbs_dbs16.pdfusesText_22

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