The pathophysiology of hypertensive acute heart failure

Abstract

While acute heart failure (AHF) is often regarded as a single disorder, an evolving understanding recognises the existence of multiple phenotypes with varied pathophysiological alterations. Herein we discuss hypertensive AHF and provide insight into a mechanism where acute fluid redistribution is caused by a disturbance in the ventricular-vascular coupling relationship. In this relationship, acute alterations in vascular elasticity, vasoconstriction and reflected pulse waves lead to increases in cardiac work and contribute to decompensated LV function with associated subendocardial ischaemia and end-organ damage. Chronic predisposing factors (neurohormonal activity, nitric oxide insensitivity, arterial stiffening) and physiological stressors (sympathetic surge, volume overload, physical exertion) that are causally linked to acute symptom onset are discussed. Lastly, we review treatment options including both nitrovasodilators and promising novel therapeutics, and discuss future directions in the management of this phenotypic variant.

Respiratory Collapse of the Inferior Vena Cava Reflects Volume Shift and Subsequent Fluid Refill in Acute Heart Failure Syndrome

“…1-3 This particular type of acute HF is characterized by an abrupt redistribution of existing fluid from the splanchnic and central circulation into the pulmonary vasculature. 2 These patients are often said to be systemically euvolemic or hypovolemic, given that acute or worsening HF can occur in the absence of significant weight gain before admission 4,5 and in the absence of significant weight reduction during admission. 6 Studies on determination of euvolemic or hypovolemic state by the direct measurement of intravascular volume are limited.…”

“Medicine of the Whole Patient”: A Modern Perusal of Classical Clinician’s Text

“…В исследовании, оце-нивающем корреляцию воспаления и снижения сосу-дистого сопряжения продемонстрирована линейная связь между маркерами воспаления (особенно С-реактивного белка) и степенью повышения жест-кости артерий [52]. Таким образом, отек легких при гипертензивной ОСН возникает в результате резкого перераспределения существующей жидкости из вис-церального и центрального кровообращения в сис-тему легочной артерии, а не вследствие увеличения объема [53].…”

Clinical and Research Considerations for Patients With Hypertensive Acute Heart Failure: A Consensus Statement from the Society of Academic Emergency Medicine and the Heart Failure Society of America Acute Heart Failure Working Group

“…[3] Such stiffening increases systolic load on the left ventricular myocardium, triggering intra-and extra-cellular adaptations that tend to normalize systolic and diastolic sarcomere stress. [1] Many of these changes occur at the expense of left ventricular compliance and ultimately lead to clinically significant diastolic dysfunction. [4] [5] As the functional ventricular-vascular relationship becomes uncoupled, the left ventricle has insufficient cardiac reserve to compensate for the increases in afterload and preload that accompany hypertensive episodes, exertion and muscle contraction.…”

“…[1] Many patients with H-AHF have a history of poorly controlled hypertension. [2] The consequences of longstanding hypertension include changes to both the vasculature as well as the ventricle, resulting in increased stiffness and reduced compliance across the cardiovascular system.…”