2007.06.27 Acute Pulmonary Edema

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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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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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


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


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

Documents

2007.06.27 Acute Pulmonary Edema