Arterial Hypertension and Flash Pulmonary Edema
High blood pressure values are recorded in almost 50% of patients with cardiogenic pulmonary edema. Not in all of these cases hypertension is the primary cause of the event but rather an associate and aggravating factor, except for “hypertensive pulmonary
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Roxana Oana Darabont
15.1 Introduction Cardiogenic pulmonary edema (CPE), also termed hydrostatic or hemodynamic edema, is a particular form of acute heart failure (AHF) characterized by the rapid accumulation of fluid within the lung’s interstitial and/or alveolar spaces as a consequence of acutely elevated cardiac filling pressures [1]. CPE occurs often in patients with underlying heart disease, but, in some situations, it can evolve even in the absence of pathologic heart conditions, like primary fluid overload. The main clinical feature of CPE is a severe, potentially fatal, acute respiratory distress. Flash pulmonary edema (FPE) is a term to describe a dramatic form of CPE with alveolar flooding. It is attributable to an excessive permeability of the pulmonary capillaries induced, on one hand, by the abrupt increase in capillary pressure that characterizes any form of CPE and, on the other hand, by a severe endothelial dysfunction caused by the excessive activation of some neurohumoral systems [2]. There are multiple pathogenic links between arterial hypertension and CPE or FPE. First of all, hypertension is the main modifiable risk factor for heart failure in developed countries [3]. The common pathway of progression from hypertension to heart failure is the concentric left ventricular hypertrophy which can induce symptomatic heart failure with preserved ejection fraction (HFpEF). Heart failure with reduced ejection fraction (HFrEF) can occur in hypertensives through the evolution of left ventricular hypertrophy to dilated cardiac failure or as a direct complication of high blood pressures, with or without an interval myocardial infarction [4]. Both forms of heart failure represent an underlying pathologic feature for CPE or FPE occurrence.
R. O. Darabont (*) Cardiology Department of University Emergency Hospital Bucharest, University of Medicine and Pharmacy “Carol Davila”, Bucharest, Romania © Springer Nature Switzerland AG 2019 M. Dorobantu et al. (eds.), Hypertension and Heart Failure, Updates in Hypertension and Cardiovascular Protection, https://doi.org/10.1007/978-3-319-93320-7_15
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Moreover, arterial hypertension is an important contributor to AHF, particularly among blacks, women, and those with HFpEF [3]. It can act as a trigger or as an associated and aggravating condition as long as excess afterload is increasing metabolic demands of the heart. Data from registries have shown that 50% of patients with AHF have a systolic blood pressure >140 mmHg at admission [5–7]. In a retrospective series of patients with CPE without severe valvular disease or nonischemic cardiomyopathies, it was found that the mean initial systolic blood pressure was 198 mmHg, confirming that high blood pressure is a common feature in this setting [8]. Not least, renal artery stenosis (RAS) is an important cause of secondary hypertension. Most patients with atherosclerotic renal artery stenosis have LVH and diastolic dysfunction as a consequence of long-lasting uncontrolled hypertension [9]. Abr
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