ACUTE PULMONARY EDEMA: -- 2/2 Cardiogenic vs Noncardiogenic Etiogloy -- Rx -- according to etiology
Appreciate the difference in mechanism of Cardiogenic and Noncardiogenc Pulmonary Edema - Mild
elevations of left atrial pressure (18 to 25 mm Hg)
cause edema in the perimicrovascular and peri-
bronchovascular interstitial spaces. As left atrial
pressure rises further (>25 mm Hg), edema fluid
breaks through the lung epithelium, flooding the
alveoli with protein-poor fluid.
- Patients with cardiogenic pulmonary edema
often have an abnormal cardiac examination. Auscultation of an S3 gallop is relatively specific for
elevated left ventricular end-diastolic pressure and
left ventricular dysfunction and suggests car-
diogenic pulmonary edema . The specificity of
this finding is high (90 to 97 percent), but its sensitivity is low (9 to 51 percent)
- Elevated
neck veins, an enlarged and tender liver, and pe-
ripheral edema suggest elevated central venous
pressure. However, assessment of central venous
pressure by physical examination in a critically ill
patient can be difficult
- Patients with noncardiogenic
edema often have warm extremities, even in the
absence of sepsis, whereas patients with cardiogenic edema and poor cardiac output usually have
cool extremities.
- In patients with
congestive heart failure, plasma BNP levels corre-
late with left ventricular end-diastolic pressure and pulmonary-artery occlusion pressure. According to a consensus panel, a BNP level below
100 pg per milliliter indicates that heart failure
is unlikely (negative predictive value, >90 percent),
whereas a BNP level greater than 500 pg per mil-
liliter indicates that heart failure is likely (positive predictive value, >90 percent). However, BNP
levels between 100 and 500 pg per milliliter provide inadequate diagnostic discrimination. BNP levels must be interpreted with caution in
critically ill patients, since the predictive value of
BNP levels is uncertain in this group. Some reports
indicate that BNP levels can be elevated in criti- dally ill patients even in the absence of heart failure. In one report,
all eight patients with sepsis with normal left
ventricular function had BNP levels above 500 pg
per milliliter. Thus, measuring BNP is most use-
ful in critically ill patients if the level is below
100 pg per milliliter. BNP levels are also higher in patients with renal failure independent of heart
failure, and a cutoff of below 200 pg per milliliter
has been suggested to exclude heart failure when
the estimated glomerular filtration rate is below
60 ml per minute. BNP is also secreted by RV, and moderate elevations have
been reported in patients with acute pulmonary
embolism, cor pulmonale, and pulmonary hypertension.
In a study of 45 patients with pulmonary
edema in whom the cause was determined clinically and with the use of sampling of pulmonary
edema fluid, a composite score based on the
radiographic features in Table 1 correctly identified 87 percent of the patients who had cardiogenic
edema and 60 percent of those who had noncar-
diogenic edema. A measurement of the width of
the vascular pedicle may improve the diagnostic
accuracy of the chest radiograph, but its utility in
distinguishing cardiogenic from noncardiogenic
edema needs further evaluation
Understanding negative pressure pulmonary edema Intensive Care Med 2014
Diffuse Pulmonary Haemorrhage CXR Shows the following CT Shows the following What is the DDx
Patient is on Coumadin, and INR is 12. Platelet is normal. Makes Anti-coag likely. But, CRP, Procalcitonin is elevated? Makes SLE less likely. Cr is normal. Vasculitis is more likely. Infection is likely as well.
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