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Interventional Therapies for Essential Hypertension
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Konstantinos P. Tsioufis, Kyriakos Dimitriadis, Alex Kasiakogias, Vassilios Papademetriou
The creation of an AV fistula results in blood flow parallel to the systemic circulation, leading to a reduction in systemic vascular resistance and cardiac afterload (15). It is well known that peripheral AV fistulae in haemodialysis patients are accompanied by decreases in BP and peripheral resistance (16,17). However, BP reduction due to the shunt in turn leads to sympathetic activation. The increase in venous return and sympathetic activation result in an increase in cardiac output. The percentage of the cardiac output that the shunt holds needs therefore to reach a threshold over which any increase in systemic resistance and cardiac output fail to maintain the baseline BP, eventually leading to its reduction. On the other hand, the increased cardiac preload leads to higher right atrial and pulmonary capillary wedge pressure that may attenuate the baroreceptor reflex (along with sympathetic activation) as well as trigger the release of natriuretic peptides. Furthermore, a central AV anastomosis reduces effective arterial blood volume to a new baseline without depleting other volume capacitance spaces, and thus without neurohormonal activation. This is of particular interest for the ageing aorta, where the stress-strain curve shifts to the left; after the anastomosis, for any increase in intravascular volume, a milder increase in BP is expected, restoring arterial compliance (18).
Systemic hypertension in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Wilbert S. Aronow, William H. Frishman
Potassium-sparing diuretics should not be given to elderly persons taking ACE inhibitors or ARBs to avoid hyperkalemia. Risk factors for renal insufficiency in older persons receiving ACE inhibitors or ARBs include renal artery stenosis (usually bilateral), polycystic renal disease, reduced absolute or effective arterial blood volume, use of nonsteroidal anti-inflammatory drugs, cyclosporine, or tacrolimus, and sepsis (91,92). However, reversible renal failure may occur in older persons treated with ACE inhibitors or ARBs who are dehydrated or salt depleted. ACE inhibitors or ARBs can cause an azotemic response when there is an absolute decrease in intravascular volume due to aggressive diuresis, poor oral intake, or gastroenteritis or an effective reduction in intravascular volume in patients with severe CHF (92).
Hyponatraemia
Published in Sherif Gonem, Ian Pavord, Diagnosis in Acute Medicine, 2017
Any cause of hypovolaemia may be accompanied by hyponatraemia. This occurs because the ADH–thirst axis, although primarily responsible for regulating body fluid osmolality, may also be activated by extreme hypovolaemia. In this circumstance, free water is retained in order to bolster the effective arterial blood volume (EABV). Thus such non-osmotic ADH release serves to maintain EABV at the expense of a reduction in osmolality.
Kidney physiology and pathophysiology during heat stress and the modification by exercise, dehydration, heat acclimation and aging
Published in Temperature, 2021
Christopher L. Chapman, Blair D. Johnson, Mark D. Parker, David Hostler, Riana R. Pryor, Zachary Schlader
Typically, the cause of AKI is divided into three pathophysiologic categories: prerenal, intrinsic, and postrenal (obstructive). AKI of prerenal origins is the most common indication of AKI and results from hypoperfusion of the kidneys occurring secondary to reductions in true or effective arterial blood volume [209]. This hypoperfusion increases RSNA, activates the renin-angiotensin-aldosterone system, and stimulates vasopressin release. Ultimately, renal blood flow and GFR are reduced and an ischemic environment is created in the renal vasculature. Intrinsic AKI is most commonly caused by ischemia or sepsis, with primary epithelial cell injury most commonly occurring in the proximal tubule [209]. The most distal S3 segment of the proximal tubule is particularly susceptible to ischemic injury [212] due to marked hypoperfusion in the medullary region and the limited ability to undergo anaerobic glycolysis [209]. Postrenal AKI is the least common type of AKI and occurs due to obstruction of the ureters, bladder outlet, or urethra [209].
Pharmacological management of portal hypertension and its complications in children: lessons from adults and opportunities for the future
Published in Expert Opinion on Pharmacotherapy, 2021
Sarah Henkel, Carol Vetterly, Robert Squires, Patrick McKiernan, James Squires
Hypervolemic or dilutional hyponatremia, defined as a reduction in serum sodium concentration to <130 mEq/L with expanded extracellular fluid volume (e.g. ascites and/or edema), is complex in its development and treatment. The proposed pathogenesis involves splanchnic vasodilatation, decreased effective arterial blood volume, and reduced glomerular filtration rate (GFR) compounded by osmotic hypersecretion of arginine vasopressin, reabsorption of water in the collecting duct, further reductions in GFR, and decreased renal synthesis of prostaglandins [48]. The development of hyponatremia portends poor outcomes in children with liver disease and thus should be aggressively managed [49]. While diuretics and fluid restriction remain the cornerstone to management, the utility of pharmacologic agents in the management of these complications in children with PHT are being explored (Table 2).
Hepatorenal syndrome: a Nationwide Trend Analysis from 2008 to 2018
Published in Annals of Medicine, 2021
Jagmeet Singh, Dushyant Singh Dahiya, Asim Kichloo, Gurdeep Singh, Katayoun Khoshbin, Hafeez Shaka
The exact pathophysiological mechanism implicated in the development of HRS is not completely understood and an area of active research, but it is believed to be secondary to renal vasoconstriction and systemic inflammation leading to impairment in renal function [5]. In patients with advanced liver disease, the development of portal hypertension leads to splanchnic vasodilation due to excessive production of vasodilators, particularly nitrous oxide [6]. This causes a significant decrease in the systemic vascular resistance thereby promoting the activation of hypotension-induced vasoconstrictor systems such as the renin-angiotensin-aldosterone system (RAAS) and Endothelin [7]. As a result, renal vasoconstriction ensues leading to decreased renal perfusion and HRS. Additionally, increased cardiac output in patients with progressive liver disease may also result in high-output cardiac failure, which induces renal vasoconstriction [2]. Furthermore, recent literature has suggested that systemic inflammation may also have a key role to play. In cirrhotics, bacterial translocation (usually gram-negative) and endotoxemia can activate the inflammatory cascade due to the release of pro-inflammatory cytokines after recognition of bacterial by-products [pathogen-associated molecular patterns (PAMS)] by immune cells [8]. This causes splanchnic vasodilation and cardiomyocyte dysfunction leading to decreased effective arterial blood volume and activation of homeostatic neurohormonal mechanisms which, in turn, decrease renal perfusion and promote the development of HRS [8].