Patient Characteristics in Flash Pulmonary Edema
Abstract & Commentary
By Michael H. Crawford, MD
Source: Dal-Bianco JP, et al. Cardiac function and brain-type natriuretic peptide in first-time flash pulmonary edema. Mayo Clin Proc. 2008;83:289-296.
Clinical features of flash pulmonary edema (PE) are poorly understood. Thus, Dal-Bianco and colleagues from the Mayo Clinic studied the records of patients coded as pulmonary edema and identified 37 patients who had first-time flash PE and an echocardiogram and a BNP level within 24 hours. Patients with a chronic heart failure exacerbation or non-cardiac PE were excluded. There were 22 women and 15 men. Left ventricular (LV) ejection fraction (EF) was reduced (< 50%) in 73%. All but three patients had coronary artery disease (CAD) alone or in combination with other cardiac diseases.
Hypertension (systolic pressure > 160) was present in 40%. Arrhythmias were present in 30%, and 22% had valvular disease. In 35%, only one of these diagnoses was present, and it was usually CAD 92%). Patients with preserved EF had significantly lower BNP values (535 vs 1320 pg/mL, P = 0.01). With the exception of EF and wall motion score, no other echo Doppler parameter was different between the two EF groups. All had elevated pulmonary artery pressure estimates (mean 47 mm Hg). Moderate-to-severe mitral regurgitation was present in about 30%. Most had evidence of elevated left ventricular filling pressures and LV diastolic dysfunction. Three-quarters of the patients had elevated troponin levels at admission, or at 6 hours after admission, and those with elevated levels had higher six-month mortality. Dal-Bianco et al concluded that CAD and hypertension are the most common antecedents to first-time flash pulmonary edema. Diastolic dysfunction is a prerequisite for flash PE and BNP levels are elevated in flash PE regardless of LVEF, but the values are lower with preserved EF.
Commentary
This retrospective analysis of first-time flash PE cases in the modern era confirms what I have been teaching house staff for years: You have to exclude myocardial ischemia. In the past, I saw too many patients get some acute treatment in the ED and be sent home. That occurs less frequently now because everyone gets a troponin drawn, but you still have to consider ischemia in initial troponin-negative patients. Although most patients had more than one potential etiology of flash PE, CAD was present in 92%. So you have to evaluate for CAD.
Despite the current epidemic of heart failure with preserved LV function; three-quarters of the patients in this series had reduced EF (< 50%). Interestingly, there were few differences in the echocardiographic, clinical, and biochemical data between the two EF groups. Although BNP was higher with reduced EF and was inversely correlated with EF, since both EF groups had similar evidence of elevated filling pressures, BNP must be strongly influenced by other factors known to affect it (age, sex, BMI, etc). Troponin levels (elevated in three-quarters of the patients) were a much better predictor of six-month mortality, even better than EF. Thus, not only is myocardial ischemia common in flash PE, the detection of ischemia/infarction is of considerable prognostic value.
Echo Doppler nicely demonstrated that the common denominator of flash PE is diastolic dysfunction and elevated LV filling pressure. Echo-Doppler E/Ea averaged 22. Values over 15 are associated with higher filling pressures. Also, Ea was < 8 in almost all patients, which indicates reduced LV relaxation. Of course, myocardial ischemia/infarction and hypertension can both reduce LV relaxation and elevate LV filling pressures.
There were some limitations to this study. It was small and retrospective. At their large center, they could only recruit 37 patients in four years. The major exclusion criteria turned out to be presentation > 6 hours after the start of symptoms. Considering that this is called flash PE, even that length of time seems generous. This confirms my experience that flash PE is unusual today. Also, the echocardiograms were obtained within 24 hours, but almost always after treatment had begun. Thus, exact conclusions about the mechanisms of onset of flash PE can only be extrapolations. However, the overall consistency of the findings argue that ischemia and high LV pressures are important mechanisms. ECG changes were not discussed in detail, but three-quarters were felt to have had a myocardial infarction.
In summary, the flash PE patient of today likely has CAD and/or hypertension; has myocardial ischemia or infarction; and usually has a low EF. I think most should have coronary arteriography, as flash PE is potentially lethal. This study was too small to evaluate the mortality rate, but I suspect it is high, especially if CAD is present.
Clinical features of flash pulmonary edema (PE) are poorly understood. Thus, Dal-Bianco and colleagues from the Mayo Clinic studied the records of patients coded as pulmonary edema and identified 37 patients who had first-time flash PE and an echocardiogram and a BNP level within 24 hours.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content