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7/28/2019 2007.06.27 Acute Pulmonary Edema
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Acute Pulmonary Edema
NEJM December 2005
Presentation: R2
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Clinical Case
A 62-year-old man presents with a three-dayhistory ofprogressive dyspnea,nonproductive cough, and low-grade fever
Congestive heart failure history
His blood pressure is 95/55 mm Hg, hisheart rate 110 beats per minute, his
temperature 37.9 degreesC, and his oxygensaturation while breathing ambient air86percent
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Clinical Case
Chest auscultation reveals rales and rhonchibilaterally
A chest radiograph showsbilateralpulmonary infiltrates consistent withpulmonary edema and borderlineenlargement of the cardiac silhouette
How should this patient be evaluated toestablish the cause of the acute pulmonaryedema and to determine appropriate therapy
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The Clinical Problem
Cardiogenic pulmonary edema (also termed
hydrostatic or hemodynamic edema)
Noncardiogenic pulmonary edema (alsoknown as increased-permeability pulmonary
edema, acute lung injury, or acute
respiratory distress syndrome)
Difficult to distinguish because of their
similar clinical manifestations
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The Clinical Problem
Cardiogenic pulmonary edema
diuretics and afterload reduction
coronary revascularization
Noncardiogenic pulmonary edemalung-protective strategy of ventilation
a low tidal volume (6 ml per kilogram of predicted bodyweight)
a plateau airway pressure less than 30 cm of waterSevere sepsis
activated protein C
low-dose hydrocortisone
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Microvascular Fluid Exchangein the Lung
Fluid and solutes that are filtered from the
circulation into the alveolar interstitial space
Do not enter the alveoli because the alveolar
epithelium is composed of very tight junctions
It moves proximally into the peribronchovascular
space
The lymphatics remove most of this filtered fluidfrom the interstitium and return it to the systemic
circulation
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Microvascular Fluid Exchangein the Lung
Increased hydrostatic pressure in thepulmonary capillaries
elevated pulmonary venous pressure
increased left ventricular end-diastolic pressureand left atrial pressure
As left atrial pressure rises further (>25 mm
Hg)edema fluid breaks through the lung epithelium
flooding the alveoli with protein-poor fluid
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Microvascular Fluid Exchangein the Lung
Noncardiogenic pulmonary edema
increase in the vascular permeability of the lung
resulting in an increased flux of fluid andprotein into the lung interstitium and air spaces
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History
Interstitial edema causes dyspnea and
tachypnea
Alveolar flooding leads to arterialhypoxemia
Cough and expectoration of frothy edema
fluid
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History
Cardiogenic pulmonary edema
ischemia with or without myocardial infarction
exacerbation of chronic systolic or diastolic heart failure,
and dysfunction of the mitral or aortic valveparoxysmal nocturnal dyspnea or orthopnea
Noncardiogenic pulmonary edema
pneumonia
sepsisaspiration of gastric contents
major trauma associated with the administration ofmultiple blood-product transfusions
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Physical Examination
Cardiogenic pulmonary edema
auscultation of an S3 gallop
a murmur consistent with valvular stenosis or
regurgitationelevated neck veins, an enlarged and tender liver, andperipheral edema
cool extremities
Noncardiogenic pulmonary edemaabdominal, pelvic, and rectal examinations areimportant
warm extremities
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Laboratory Testing
Electrocardiography
Elevated troponin levels
Measurement of electrolytes, the serumosmolarity, and a toxicology screen
Serum amylase and lipase
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Laboratory Testing
BNP is secreted predominantly by the cardiac
ventricles in response to wall stretch or increased
intracardiac pressures
BNP level below 100 pg per milliliter indicatesthat heart failure is unlikely (negative predictive
value, >90 percent)
BNP level greater than 500 pg per milliliterindicates that heart failure is likely (positive
predictive value, >90 percent)
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Laboratory Testing
BNP levels between 100 and 500 pg per milliliter
provide inadequate diagnostic discrimination
BNP can also be secreted by the right ventricle,
and moderate elevations have been reported inpatients with acute pulmonary embolism, cor
pulmonale, and pulmonary hypertension
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Chest Radiography
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Echocardiography
The first approach to assessing leftventricular and valvular function in patientsin whom the history, physical and laboratory
examinations, and the chest radiograph donot establish the cause of pulmonary edema
Less sensitive in identifying diastolic
dysfunctionDoes not rule out cardiogenic pulmonaryedema
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Pulmonary-ArteryCatheterization
Assess thepulmonary-artery occlusion pressure
Is considered the gold standard for determining the
cause of acute pulmonary edema
Monitoring of cardiac filling pressures, cardiac
output, and systemic vascular resistance
Common complications included hematoma at the
insertion site, arterial puncture, bleeding,arrhythmias, and bloodstream infection
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Measurement ofcentral venous pressure
should not be considered a valid substitute
for pulmonary-artery catheterization
available data suggest that there is often a poor
correlation between the two
acute or chronic pulmonary arterial
hypertension and right ventricular overloadin the absence of any increase in left atrial
pressure
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Stepwise Approach
The noninvasive approaches for diagnosis
will inevitably lead to the misclassification
of some patients
repeated and ongoing assessment is necessary
requiring simultaneous diagnosis and treatment
10 percent of patients with acute pulmonary
edema have multiple causes of edema
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Guidelines
There are currently no published guidelines
from professional societies between
cardiogenic and noncardiogenic pulmonary
edema
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Conclusions andRecommendations
Treatment can be provided while thediagnostic steps are taken
begin with a careful history and physical
examinationelectrocardiogram
measurement of plasma BNP
chest radiograph
transthoracic echocardiogram
pulmonary-artery catheter
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Thanks for your attention