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Diabetic Nephropathy
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The balance of sodium and water is maintained by increased fractional sodium excretion in the urine, plus a normal thirst response. Plasma sodium is usually normal. Hypervolemia usually occurs when dietary intake of sodium or water is restricted or excessive. Heart failure may be caused by an overload of sodium and water. This is more common if the patient has decreased cardiac reserve. Potassium is a substance with secretion mostly controlled via distal nephron secretion. Therefore, renal adaptation usually regulates normal plasma levels of potassium. This cannot occur when renal failure is advanced or the patient consumes too much potassium in the diet. Plasma potassium can be increased when renal failure is not as advanced by the use of ACE inhibitors, potassium-sparing diuretics, beta-blockers, cyclosporine, NSAIDs, tacrolimus, pentamidine, trimethoprim/sulfamethoxazole, or ARBs.
Body fluids and electrolytes
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
A person with acute hypervolaemia may present with shortness of breath, cough and orthopnoea, with an elevated blood pressure, tachycardia and a bounding pulse. Chest auscultation may reveal an expiratory wheeze, and inspiratory crackles may also be audible. The neck veins may be distended. If the patient is being haemodynamically monitored, their central venous pressure (CVP) will be elevated. For causes of hypervolaemia see Table 4.5. If left untreated, hypervolaemia can progress to acute pulmonary oedema, which is a medical emergency (see Chapter 6).
SBA Answers
Published in Justin C. Konje, Complete Revision Guide for MRCOG Part 2, 2019
A Restriction of fluid intake and consider starting a diureticWhere excessive systemic absorption of fluid distension media is suspected, strict fluid balance monitoring should be commenced, a urinary catheter inserted and serum electrolytes measured. If the patient develops signs of cardiac failure and or pulmonary oedema, then a cardiac echocardiogram and chest X-ray should be undertaken. Asymptomatic hypervolaemia with or without hyponatraemia should be managed by fluid restriction with or without diuretics. The management of symptomatic hypovolaemic hyponatraemia requires a multidisciplinary involvement including anaesthetist, physicians and intensivisits in a high dependency or intensive care unit. (Umranikar S et al. BSGE/ESGE guideline on management of fluid distension media in operative hysteroscopy. The Obstetrician & Gynaecologist 2018; 20:197–200)
The role of serial cardiac biomarkers in prognostication and risk prediction of chronic heart failure: additional scientific insights with hemodynamic feedback
Published in Expert Review of Cardiovascular Therapy, 2023
Youssra Allach, Jasper J. Brugts
The pathophysiology of HF is greatly influenced by the activation of the neurohormonal system. In order to keep the cardiovascular system in a state of homeostasis, the regulation of the blood volume in circulation is closely controlled by the neurohormonal system. The aorta and carotid sinus contain what are known as baroreceptors, which are able to detect changes in the arterial blood volume of the peripheral circulation. While the carotid sinus’s baroreceptors detect high pressure, those in the aortic arch operate as low-pressure cardiopulmonary mechanoreceptors. When engaged, the baroreceptors have an inhibitory impact on the central nervous system and suppress systemic circulation and outflow to the heart. Changes in the heart’s ability to pump blood, the amount of blood circulating in the body, or both cause a drop-in baroreceptor activity. Parasympathetic tone decreases as a result, and sympathetic tone is reflexively enhanced [18,19]. This causes an increase in heart rate and contractility as well as peripheral vasoconstriction. Additionally, neurohormonal stimulation can result in renal salt retention, which can result in hypervolemia. The effects of diuretics are exacerbated, and their effectiveness is decreased when renal impairment is present [20]. Therefore, the extent of neurohormonal activity in HF has been found to be correlated with the severity of the condition and the clinical prognosis [21].
Thiazide-associated hyponatremia in internal medicine patients: analysis of epidemiological and biochemical profiles
Published in Postgraduate Medicine, 2022
Since TAH is considered to occur mostly in normovolemic conditions [12,23], the analysis of volume status of TAH patients revealed a surprisingly large group of patients (32.9%) with signs of volume depletion. And this proportion could be possibly higher as we included only patients with osmolality < 280 mmol/kg. Thus, patients with severe hypovolemia, leading to renal failure and increased s-urea, could be excluded even if their effective osmolality is low and they suffer from the true hyponatremia [28]. Only a minority of our patients (2.1%) were classified as hypervolemic and we attribute this mostly to the absence of the two main causes of hypotonic hypervolemic hyponatremia: the ADHF and ascites. A majority of patients with ADHF, that is complicated by hypotonic hyponatremia, are mostly admitted to the Cardiology Department instead of the Internal Medicine Department, and pharmacotherapy of ascites does not usually include thiazide [29].
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).