The patient is a 56-year-old female whose prior medical history was notable only for hypertension. She had noted mild paroxysmal nocturnal dyspnea and exertional dyspnea but otherwise was in good health. On the night of admission she went to the bathroom and returned stating “I can’t breathe”. Her husband noted she was severely short of breath and diaphoretic. Emergency medical services was contacted, and shortly after arrival in the emergency department she required intubation.
After intubation, 100% inspired oxygen and increasing levels of positive expiratory pressure to 10 mmHg resulted in oxygen saturations of only 85-90%. Physical exam was notable for a blood pressure of 85/60 mmHg, a heart rate of 110 bpm, temperature 97.6 F, diffuse wheezing, distant heart sounds without obvious murmur, and intact pulses.
The initial chest x-ray (Figure 1) demonstrated the endotrachial tube to be in good position. The initial electrocardiogram demonstrated sinus tachycardia, without ischemic ST-T wave changes.
| Lab Values |
| Creatinine |
Normal |
| WBC |
25,000 x 106 with left shift |
| Hgb |
11.3 g/dL (normal 13.3-17.3 g/dL) |
| TnI (initial) |
<0.6 (normal <1.0 ng/ml) |
| CK-MB (Initial) |
1.9 ng/ml (normal < 8 ng/ml) |
| BNP (initial) |
350 pg/ml (normal < 80 pg/ml) |
|
| |
| BNP (2 hours) |
228 pg/ml (normal < 80 pg/ml) |
| TnI (9 hours) |
1.8 ng/ml (normal <1.0 ng/ml) |
| CK-MB (9 hours) |
2.3 ng/ml (normal < 8 ng/ml) |
|
There was almost complete opacification of both lungs. The radiologist interpretation was severe bilateral airspace disease, most consistent with acute respiratory distress syndrome or diffuse pneumonia.
The correct answer is: D. Acute cardiogenic pulmonary edema
Choice A, pneumonia, is unlikely, due to the acute onset of symptoms and lack of fever. However, given the elevated white blood cell count, assessing blood cultures and initiating antibiotics appear reasonable.
Choice B, non-cardiogenic pulmonary edema, is unlikely given the acute time course of the hypoxia. Common causes of non-cardiogenic pulmonary edema include pneumonia (see A), trauma, blood transfusion, or aspiration.
Choice C, pulmonary embolism, is always a consideration in a patient with acute dsypnea. However, commonly the chest x-ray would not demonstrate significant abnormalities. Although concomitant pulmonary embolism is always a consideration, given the extensive lung findings, this would be unlikely.
This leaves D, cardiogenic pulmonary edema as the most likely cause. In this case, emergent performance of echocardiography is valuable. The patient has clinical findings consistent with cardiogenic shock, but the ECG is not consistent with acute myocardial infarction. Echocardiography can assist in determining if there is significant left ventricular dysfunction, or an acute mechanical problem.
Case course:
The patient was admitted to the coronary care unit for further therapy. Based on the chest x-ray findings, blood cultures were drawn and broad-spectrum antibiotics were initiated. Subsequently, hypotension necessitated initiation of vasopressor support with dopamine. A transthoracic echocardiogram was performed, but due to suboptimal images, a transesophageal echocardiogram was then performed. This demonstrated normal systolic function without obvious wall motion abnormalities. In addition, there was a partially flail anterior mitral valve leaflet (view video 1) with associated severe mitral regurgitation (view video 2). A pulmonary artery catheter was inserted which demonstrated a significantly elevated wedge pressure with large V-waves. Intravenous nesiritide was initiated with good response with normalization of the systolic blood pressure and decrease in the wedge pressures. An intra-aortic balloon pump was placed, and coronary angiography was performed, which demonstrated no significant disease. The patient underwent successful mitral valve replacement 48 hours after admission, and was subsequently discharged home 8 days postoperatively.
Discussion:
Although BNP levels have been reported to have a high sensitivity and negative predictive value for CHF, in this patient BNP was surprisingly low, and in the range commonly seen in patients with primarily right-sided abnormalities or mild CHF, rather than those who have severe CHF.
High BNP values are useful for ruling in heart failure, while low levels are useful for excluding it. However, there remains a “gray zone” in which values are not as useful, as elevations may result from conditions other the systolic dysfunction. In these cases, consideration of the clinical presentation, rather than relying on laboratory tests, is critical for proper diagnosis.
BNP values have been reported to be normal or lower than expected in patients with heart failure in a number of situations. If the patient presents early, BNP may not have had time to increase (1). Well compensated heart failure may have low BNP values (2). In addition, it has been hypothesized that in the setting of long standing systolic dysfunction that the left ventricle has impaired ability to synthesize and secrete BNP, resulting in low levels despite severe systolic dysfunction and elevated wedge pressures. Finally, any condition that results in unloading of the left ventricle with concomitant increased left atrial pressure may result in low BNP values despite pulmonary edema, such as mitral stenosis, or in this case, hyperdynamic systolic function and severe mitral regurgitation.
References
- Logeart D, Saudubray C, Beyne P, et al. Comparative value of Doppler echocardiography and B-type natriuretic peptide assay in the etiologic diagnosis of acute dyspnea. J Am Coll Cardiol 2002;40:1794-80.
- Tang WH, Girod JO Lee MJ, et al. Plasma B-type natriuretic peptide levels in ambulatory patients with established chronic symptomatic systolic heart failure. Circulation 2003;108;2964-66.
Log in to MyACC
