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Chronic hypertension and acute hypertensive crisis
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
William F. Rayburn, Lauren Plante
The pathophysiology of hypertensive crisis is still inadequately understood. Because blood pressure is determined by cardiac output and peripheral vascular resistance, and cardiac output itself is a product of heart rate and stroke volume, there are several possible triggers, but it appears that an abrupt increase in systemic vascular resistance is most commonly involved (53). Mechanical stress causes vascular endothelial damage, which in turn provokes increased permeability, activation of the coagulation cascade, and fibrin deposition. Fibrinoid necrosis of the arterioles can further decrease vascular perfusion and thus activate the mediators commonly associated with ischemia, further worsening injury. In many (but not all) hypertensive crises, the renin–angiotensin system is activated, forcing further vasoconstriction and production of inflammatory cytokines (59). Because of pressure natriuresis, effective circulating volume is decreased: this stimulates the kidney to produce vasoconstrictive mediators. A feed-forward loop or vicious circle becomes difficult to break.
Critical care, neurology and analgesia
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
The most obvious alteration to pharmacokinetics occurs on initiation of ECMO, when the patients own blood volume mixes with the priming volume in the extracorporeal circuit. For example, on initiation of ECMO the effective circulating volume will be almost doubled in neonates. One possible effect of this acute haemodilution is a decrease in the total blood concentration of any drug present. The pharmacological impact will depend on the apparent volume of distribution of the drug, the degree of protein binding and the extent of equilibration between tissue concentrations and plasma concentrations on initiation of ECMO.
Investigation of Pituitary Disease
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Thozhukat Sathyapalan, Stephen L. Atkin
Urinary sodium concentration is helpful when the cause of hyponatraemia is not apparent from the history and examination or when SIADH is suspected. In euvolaemic hyponatraemia (including SIADH), the urinary sodium is ≥30 mmol/L.22, 25 Hypervolaemic hyponatraemia should be apparent clinically; because of the reduced effective circulating volume, the kidney concentrates the urine (>100 mOsm/kg) and conserves sodium (<30 mmol/L; but it can be higher when the patient is taking diuretics).22 The clues to hypovolaemia in the history include obvious fluid loss (through diuretics, for example) or third space fluid loss, when fluid with high sodium content is sequestered in a body space, as occurs in burns patients. The urinary sodium concentration in all hypovolaemic hyponatraemia is <30 mmol/L except when the kidney is the site of the loss, for example with diuretic use, salt-losing nephropathy, or mineralocorticoid deficiency.26
Nonsteroidal anti-inflammatory drugs in end-stage kidney disease: dangerous or underutilized?
Published in Expert Opinion on Pharmacotherapy, 2021
NSAID-related adverse kidney outcomes are similarly well documented. Inhibition of prostaglandin synthesis, particularly of prostaglandin E2 (PGE2) and PGI2, has the net effect of increased sodium reabsorption in the thick ascending loop of Henle and decreased potassium secretion in the distal tubule leading to hyperkalemia and a Type IV renal tubular acidosis [36–38]. Increased sodium and water retention, in turn, is thought to contribute to mild worsening of blood pressure control and decreased response to antihypertensive agents, particularly loop diuretics [36,39]. Acute kidney injury (AKI) is a common complication of NSAID therapy as well, with NSAID-associated AKI accounting for up to 15.5% of all cases of drug-related kidney failure [40,41]. PGI2 is essential in maintaining adequate kidney perfusion in patients with other preexisting health conditions that predispose to decreased actual or effective circulating volume [36]. NSAID use in these individuals may increase the risk of ischemia and acute tubular necrosis. Long-term consumption of NSAIDs is also known to cause analgesic nephropathy, the hallmarks of which are renal papillary necrosis and chronic kidney dysfunction [36,42]. Finally, two rare complications of NSAID therapy are interstitial nephritis and minimal change disease [36,43,44]. While the mechanism of this association is currently unknown, it is hypothesized that COX inhibition shunts arachidonic acid down alternate metabolic pathways to produce pro-inflammatory prostanoids [36].
Pharmacotherapeutic principles of fluid management in heart failure
Published in Expert Opinion on Pharmacotherapy, 2021
Bharat Narasimhan, R. Aravinthkumar, Ashish Correa, Wilbert S. Aronow
Interestingly, body weight appears to correlate poorly with deteriorating cardiac function preceding ADHF [17]. Further study of this phenomenon indicates that volume redistribution is an important contributing mechanism to decompensation. Redistribution within the vascular compartment is largely via the splanchnic circulation that contains between 20% and 50% of the circulating blood volume. The high compliance of this vascular bed allows it to dynamically impact the effective circulating volume. The rich sympathetic innervation of the splanchnic vasculature permits a brisk vasomotor response with up to 50% increase in preload with adrenergic stimulation [18]. This is of particular importance in HF where increased NH activation has been implicated in potentially decreasing splanchnic capacitance thereby increasing the effective preload. Furthermore, sympathetic stimulation during exercise is hypothesized to similarly contribute to increase cardiac workload culminating in a decreased exercise tolerance.
The role of the clinical laboratory in diagnosing acid–base disorders
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
The normal kidney can excrete large amounts of HCO3− and accordingly, metabolic alkalosis can occur only when both an increase in alkali and impairment in renal HCO3− excretion exist [2,122,123]. The majority of patients with metabolic alkalosis have gastric fluid loss or diuretic use, either long-acting thiazide diuretics, or multiple doses of short-acting loop diuretics (Figure 2). If the patient does not vomit or use diuretics, the pathophysiology is often related to increased renin–angiotensin–aldosterone activity. In most secondary cases, aldosterone is required to adjust to volume depletion and the blood pressure will be low. Aldosterone promotes sodium retention in exchange for excretion of potassium or hydrogen, resulting in metabolic alkalosis and often also hypokalemia. The blood pressure will be high in case of primary hyperaldosterism or pseudohyperaldosteronism, including high intake of licorice that has aldosterone characteristics [124–126]. By using the urine [Cl−], one can distinguish between Cl−-responsive and Cl−-resistant metabolic alkalosis. If the kidneys perceive a reduced “effective circulating volume,” they avidly reabsorb filtered Na+, HCO3−, and Cl−, largely via activation of the renin–angiotensin–aldosterone system, thus reducing urine [Cl−] [2,118]. A (spot) urine [Cl−] < 10 mmol/L will be reflective of the so-called chloride responsive metabolic alkalosis because administration of fluids with NaCl (usually with KCl) restores effective arterial volume and/or K+ deficiency with correction of metabolic alkalosis [122,123,126,127].