Hemodynamic Mechanisms
It is of importance to better understand the pathophysiological mechanisms leading to left ventricular (LV) maladaptation and the timely identification and management of patients at risk for developing symptomatic heart failure (HF). High blood pressure i
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Hemodynamic Mechanisms Tatiana Kuznetsova and Nicholas Cauwenberghs
4.1
Introduction
The normal heart is an efficient muscle that is designed to serve both as pump and integrator of two independent vascular systems, the pulmonary and systemic circulations. The capacity of the body to augment cardiac output, regulate systemic blood pressure (BP), and respond appropriately to elevations in heart rate and pre- and afterload depends on the properties of both the heart and the vasculature into which the left ventricle (LV) ejects blood [1]. Two components of systemic BP could be identified: the steady component, represented by mean arterial pressure, and the pulsatile component, represented by pulse pressure. Mean arterial pressure is determined by peripheral arterial resistance, which depends on the physical characteristics of the arterial tree and the volume of blood that the LV ejects. On the other hand, LV stroke volume and aortic compliance are major determinates of pulse pressure. In the absence of aortic stenosis, conventionally measured brachial BP provides a clinically useful estimate of LV afterload. When a high afterload opposes LV ejection, reduction of the LV stroke volume could be observed in a short term. This reduction is further compensated by shifting the LV pump function to a higher energy level (the Frank-Starling mechanism) and by activating an autoregulatory mechanism (the Anrep response). However, the longterm increased afterload and, consequently, the chronically increased cardiac performance lead to adverse LV remodeling and dysfunction and increased LV oxygen requirements and eventually cause symptomatic heart failure (HF). Because the process of myocardial remodeling/dysfunction starts long before the onset of symptomatic HF, it is of importance to better understand the pathophysiological mechanisms leading to subclinical (asymptomatic) LV maladaptation and the timely identification T. Kuznetsova (*) · N. Cauwenberghs Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium e-mail: [email protected]; [email protected] © 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_4
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of patients who are at risk for developing overt cardiac events. Hereby we discussed the different aspects of cardiac maladaptive responses to a chronically increased load.
4.2
LV Deformation
LV deformation (strain) is determined by the fiber structure and curvature of the myocardium and its interaction with local wall stress at the beginning of ejection, which decreases from the endocardium to epicardium and from the LV base to the apex [2]. During LV ejection, longitudinal deformation of the heart results from contraction of longitudinally oriented subendocardial and subepicardial fibers, whereas radial LV wa
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