Pulmonary edema prognostic score predicts in-hospital mortality risk in patients with acute cardiogenic pulmonary edema Marcin Fiutowski, MD, PhD, a Tomasz Waszyrowski, MD, PhD, a Maria Krzemin ´ ska-Pakula, MD, PhD, b and Jaroslaw D. Kasprzak, MD, PhD b BACKGROUND: Congestive heart failure is a common cardiac disorder associated with a high mor- tality. There are a limited number of prognostic scales predicting in-hospital outcomes after an acute episode of congestive heart failure. OBJECTIVES: The goal of this investigation was to develop a simple prognostic score predicting in-hospital outcome in patients with acute cardiogenic pulmonary edema. METHODS: We retrospectively studied 276 consecutive patients hospitalized with acute pulmonary edema from the years 1998 to 2000. RESULTS: During the initial hospitalization, 58 patients (21%) died and 218 patients (79%) were discharged. Statistical analyses revealed that the most significant predictors of inhospital mortality were acute myocardial infarction, heart rate greater than 115/beats/min, systolic blood pressure of 130 mm Hg or less, and white blood cell count greater than 11,500/mm 3 on presentation. The presence of each factor was scored as 1 point, and the absence was scored as 0 points. The Pulmonary Edema Prognostic Score (PEPS) was defined as a sum of all points. Patients with a PEPS of 0 had good short-term prognosis with a 2% in-hospital mortality rate, whereas mortality in patients with a PEPS of 4 was 64%. CONCLUSIONS: The PEPS is a simple tool that can be easily calculated using common clinical diagnostic tests (electrocardiogram, blood pressure, heart rate, and white cell count) to determine in-hospital mortality risk in patients with an acute episode of cardiogenic pulmonary edema. (Heart Lung® 2008;37:46 –53.) A cute cardiogenic pulmonary edema is the manifestation of systolic and/or diastolic car- diac dysfunction and is a common reason for acute in-patient hospitalization. The hallmark of acute pulmonary edema is an increased pulmonary capillary pressure attributed to systolic and/or dia- stolic left ventricular dysfunction. Cardiogenic pul- monary edema is associated with neurohormonal activation and endothelial barrier dysfunction in concert with the elevated pulmonary capillary pres- sure that forces capillary fluid into the pulmonary interstitial and alveolar space. A widely accepted, contemporary view of the mechanisms of pulmo- nary edema emphasizes the importance of fluid re- distribution associated with heart failure. This the- ory explains the lung hyperemia, impaired perfusion of other organs, and pre-renal, renal failure fre- quently observed during acute pulmonary edema. 1-9 Myocardial infarction is the most frequent cause of heart failure and pulmonary edema. Myocardial muscle injury results in an inadequate cardiac func- tional reserve and elevation in left ventricular dia- stolic, venous, and pulmonary capillary pressure. An increased preload caused by fluid retention and in- creased afterload caused by vasoconstriction, together with cardiac arrhythmia or conduction abnormalities, decrease cardiac function. All of these alterations re- distribute fluid from the pulmonary capillaries to the pulmonary interstitial and alveolar space. 5 From the a Department of Cardiology, Jonscher Hospital, Milion- owa 14, Poland; and b II Chair and Department of Cardiology, Medical University of Lódz ´, Biegan ´ ski Hospital, Kniaziewicza 1/5, Poland. Reprint requests: Marcin Fiutowski, MD, PhD, Department of Cardiology, Jonscher Hospital, 93-113 Lódz ´, Milionowa 14, Poland. 0147-9563/$ – see front matter Copyright © 2008 by Mosby, Inc. doi:10.1016/j.hrtlng.2007.05.005 46 www.heartandlung.org JANUARY/FEBRUARY 2008 HEART & LUNG