Concept of Fluid Balance and Pathophysiology

Concept of Fluid Balance and Pathophysiology ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS ON Concept of Fluid Balance and Pathophysiology As a learner in Pathophysiology, it’s important to take the information you are absorbing from your coursework and connect it to real life. Throughout the semester you will be invited to make connections by locating, reviewing, and summarizing current and relevant journal articles. Concept of Fluid Balance and Pathophysiology Use the following link to learn how to find and evaluate an online source: (Links to an external site.) Please follow the instructions below: Locate a current (medical or scientific) news or journal article based on one of the topics listed below: Distribution of body fluids and Electrolytes (Chapter 5, p. 114), Alterations in Potassium & other Electrolytes (Ch 5, P. 122) Note: As you read through the article, think about how it connects to Pathophysiology and why is it relevant. Provide a write-up summarizing the article. Within your document, include how the information connects to Pathophysiology, and why it is relevant. Aim to include 150 – 200 words in the summary. Remember to cite your source(s) in APA Format! attachment_1 School of Nursing and Midwifery Mount Royal University Calgary, Alberta U.S. AUTHORS Sue E. Huether, MS, PhD Professor Emeritus College of Nursing University of Utah Salt Lake City, Utah Kathryn L. McCance, MS, PhD Professor Emeritus College of Nursing University of Utah Salt Lake City, Utah U.S. Section Editors Valentina L. Brashers, MD Professor of Nursing and Woodard Clinical Scholar Attending Physician in Internal Medicine University of Virginia Health System Charlottesville, Virginia Neal S. Rote, PhD Academic Vice-Chair and Director of Research Department of Obstetrics and Gynecology University Hospitals Case Medical Center William H. Weir, MD, Professor of Reproductive Biology and Pathology Case Western Reserve University School of Medicine 3 102. Shennan T. Postmortems and morbid anatomy. 3rd ed. William Wood: Baltimore; 1935. 103. Riley MW. Foreword: the gender paradox. Ory MG, Warner HR. Gender, health, and longevity: multidisciplinary perspectives. Springer: New York; 1990. 104. Katsumata Y, Sato K, Yada S. Green pigments in epidermal blisters of decomposed cadavers. Forensic Science International. 1985;28(3–4):167–174. 364 5 Fluids and Electrolytes, Acids and Bases Sue E. Huether, Stephanie Zettel CHAPTER OUTLINE Distribution of Body Fluids and Electrolytes, 115 Water Movement Between Plasma and Interstitial Fluid, 115 Water Movement Between ICF and ECF, 116 Alterations in Water Movement, 116 Edema, 116 Sodium, Chloride, and Water Balance, 117 Alterations in Sodium, Chloride, and Water Balance, 120 Isotonic Alterations, 121 Hypertonic Alterations, 121 Hypotonic Alterations, 121 Alterations in Potassium and Other Electrolytes, 122 Potassium, 122 Other Electrolytes—Calcium, Phosphate, and 365 Magnesium, 126 Acid-Base Balance, 126 Hydrogen Ion and pH, 126 Buffer Systems, 126 Acid-Base Imbalances, 128 PEDIATRIC CONSIDERATIONS: Distribution of Body Fluids, 132 GERIATRIC CONSIDERATIONS: Distribution of Body Fluids, 132 The cells of the body live in a fluid environment with electrolyte and acid-base concentrations maintained within a narrow range. Changes in electrolyte concentration affect the electrical activity of nerve and muscle cells and cause shifts of fluid from one compartment to another. Alterations in acid-base balance disrupt cellular functions. Fluid fluctuations also affect blood volume and cellular function. Disturbances in these functions are common and can be life-threatening. Understanding how alterations occur and how the body compensates or corrects the disturbance is important for comprehending many pathophysiological conditions. Distribution of Body Fluids and Electrolytes The sum of fluids within all body compartments constitutes total 366 body water (TBW)—about 60% of body weight in adults (Table 51). The volume of TBW is usually expressed as a percentage of body weight in kilograms. One litre of water weighs 1 kg. The rest of the body weight is composed of fat and fat-free solids, particularly bone. TABLE 5-1 Total Body Water (%) in Relation to Body Weight Body Build Adult Male Adult Female Child (1–10 yr) Infant (1 mo–1 yr) Newborn (Up to 1 mo) Normal Lean Obese 60 70 50 50 60 42 65 50-60 50 70 80 60 70–80 NOTE: Total body water is a percentage of body weight. mo, month; yr, year. Body fluids are distributed among functional compartments, or spaces, and provide a transport medium for cellular and tissue function. Intracellular fluid (ICF) comprises all the fluid within cells, about two thirds of TBW. Extracellular fluid (ECF) is all the fluid outside the cells (about one third of TBW) and includes interstitial fluid (the space between cells and outside the blood vessels) and intravascular fluid (blood plasma) (Table 5-2). The total volume of body water for a 70-kg person is about 42 litres. Concept of Fluid Balance and Pathophysiology Other ECF compartments include lymph and transcellular fluids, such as synovial, intestinal, and cerebrospinal fluid; sweat; urine; and pleural, peritoneal, pericardial, and intraocular fluids. TABLE 5-2 Distribution of Body Water (70-kg Man) Fluid Compartment % of Body Weight Volume (L) Intracellular fluid (ICF) Extracellular fluid (ECF) Interstitial Intravascular Total body water (TBW) 40 20 15 5 60 28 14 11 3 42 Electrolytes and other solutes are distributed throughout the intracellular and extracellular fluid (Table 5-3). Note that ECF contains a large amount of sodium and chloride and a small amount 367 of potassium, whereas the opposite is true of ICF. The concentrations of phosphates and magnesium are greater in ICF, and the concentration of calcium is greater in ECF. These differences are important for the maintenance of electroneutrality between the extracellular and intracellular compartments, the transmission of electrical impulses, and the movement of water among body compartments (see Chapter 1). TABLE 5-3 Representative Distribution of Electrolytes in Body Compartments Electrolytes Cations Sodium Potassium Calcium Magnesium TOTAL Anions Bicarbonate Chloride Phosphate Proteins Other anions TOTAL ECF (mmol/L) ICF (mmol/L) 142 4.2 2.5 1 149.7 12 150 0 12 174 24 103 2 16 8 153 12 4 100 65 6 187 ECF, extracellular fluid; ICF, intracellular fluid. Although the amount of fluid within the various compartments is relatively constant, solutes (e.g., salts) and water are exchanged between compartments to maintain their unique compositions. The percentage of TBW varies with the amount of body fat and age. Because fat is water repelling (hydrophobic), very little water is contained in adipose (fat) cells. Individuals with more body fat have proportionately less TBW and tend to be more susceptible to dehydration. The distribution and the amount of TBW change with age (see the Pediatric Considerations and Geriatric Considerations boxes later in this chapter), and although daily fluid intake may fluctuate widely, the body regulates water volume within a relatively narrow range. Water obtained by drinking, water ingested in food, and water derived from oxidative metabolism are the primary sources of body water. Normally, the largest amounts of water are lost through renal excretion, with lesser amounts lost through the stool and 368 vaporization from the skin and lungs (insensible water loss) (Table 5-4). TABLE 5-4 Normal Water Gains and Losses (70-kg Man) Daily Intake (mL) Daily Output (mL) Drinking Water in food Water of oxidation 1 400–1 800 700–1 000 300–400 Urine Stool Skin Lungs TOTAL 2 400–3 200 TOTAL 1 400–1 800 100 300–500 600–800 2 400–3 200 Water Movement Between Plasma and Interstitial Fluid The distribution of water and the movement of nutrients and waste products between the capillary and interstitial spaces occur as a result of changes in hydrostatic pressure (pushes water) and osmotic or oncotic pressure (pulls water) at the arterial and venous ends of the capillary (see Figure 1-24). Concept of Fluid Balance and Pathophysiology Water, sodium, and glucose readily move across the capillary membrane. The plasma proteins normally do not cross the capillary membrane and maintain effective osmolality by generating plasma oncotic pressure (particularly albumin). As plasma flows from the arterial to the venous end of the capillary, four forces determine whether fluid moves out of the capillary and into the interstitial space (filtration) or whether fluid moves back into the capillary from the interstitial space (reabsorption). These four forces acting together are described as net filtration or Starling forces: 1. Capillary hydrostatic pressure (blood pressure) facilitates the outward movement of water from the capillary to the interstitial space. 2. Capillary (plasma) oncotic pressure osmotically attracts water from the interstitial space back into the capillary. 3. Interstitial hydrostatic pressure facilitates the inward movement of water from the interstitial space into the capillary. 369 4. Interstitial oncotic pressure osmotically attracts water from the capillary into the interstitial space. The forces moving fluid back and forth across the capillary wall are summarized as follows: At the arterial end of the capillary, hydrostatic pressure exceeds capillary oncotic pressure and fluid moves into the interstitial space (filtration). At the venous end of the capillary, capillary oncotic pressure exceeds capillary hydrostatic pressure and fluids are attracted back into the circulation (reabsorption). Interstitial hydrostatic pressure promotes the movement of about 10% of the interstitial fluid along with small amounts of protein into the lymphatics, which then returns to the circulation. Because albumin does not normally cross the capillary membrane, interstitial oncotic pressure is normally minimal. Figure 5-1 illustrates net filtration. 370 Net Filtration—Fluid Movement Between Plasma and Interstitial Space. The movement of fluid between the vascular, interstitial spaces and the lymphatics is the result of net filtration of fluid across the semipermeable capillary membrane. Capillary hydrostatic pressure is the primary force for fluid movement out of the arteriolar end of the capillary and into the interstitial space. At the venous end, capillary oncotic pressure (from plasma proteins) attracts water back into the vascular space. Interstitial hydrostatic pressure promotes the movement of fluid and proteins into the lymphatics. Osmotic pressure accounts for the movement of fluid between the interstitial space and the intracellular space. Normally, intracellular and extracellular fluid osmotic pressures are equal (280 to 294 mOsm) and water is equally distributed between the interstitial and intracellular compartments. FIGURE 5-1 Water Movement Between ICF and ECF Water moves between ICF and ECF compartments primarily as a function of osmotic forces. Water moves freely by diffusion through the lipid bilayer cell membrane and through aquaporins, a family of water channel proteins that provide permeability to water.1 371 Sodium is responsible for the ECF osmotic balance, and potassium maintains the ICF osmotic balance. The osmotic force of ICF proteins and other nondiffusible substances is balanced by the active transport of ions out of the cell. Water crosses cell membranes freely, so the osmolality of TBW is normally at equilibrium. Normally ICF is not subject to rapid changes in osmolality, but when ECF osmolality changes, water moves from one compartment to another until osmotic equilibrium is reestablished (see “Isotonic Alterations,” p. 121). Alterations in Water Movement Edema Edema is excessive accumulation of fluid within the interstitial spaces. The forces favouring fluid movement from the capillaries or lymphatic channels into the tissues are increased capillary hydrostatic pressure, decreased plasma oncotic pressure, increased capillary membrane permeability, and lymphatic channel obstruction2 (Figure 5-2).Concept of Fluid Balance and Pathophysiology FIGURE 5-2 Mechanisms of Edema Formation. H2O, water; Na+, sodium. 372 Pathophysiology Capillary hydrostatic pressure increases as a result of venous obstruction or salt and water retention. Venous obstruction causes hydrostatic pressure to increase behind the obstruction, pushing fluid from the capillaries into the interstitial spaces. Thrombophlebitis (inflammation of veins), hepatic obstruction, tight clothing around the extremities, and prolonged standing are common causes of venous obstruction. Heart failure, renal failure, and cirrhosis of the liver are associated with excessive salt and water retention, which cause plasma volume overload, increased capillary hydrostatic pressure, and edema. Since plasma albumin acts like a magnet to attract water, loss or diminished production (e.g., from liver disease or protein malnutrition) contributes to decreased plasma oncotic pressure. Plasma proteins are lost in glomerular diseases of the kidney, serous drainage from open wounds, hemorrhage, burns, and cirrhosis of the liver. The decreased oncotic attraction of fluid within the capillary causes filtered capillary fluid to remain in the interstitial space, resulting in edema. Capillaries become more permeable with inflammation and immune responses, especially with trauma such as burns or crushing injuries, neoplastic disease, and allergic reactions. Proteins escape from the vascular space and produce edema through decreased capillary oncotic pressure and interstitial fluid protein accumulation. The lymphatic system normally absorbs interstitial fluid and a small amount of proteins. When lymphatic channels are blocked or surgically removed, proteins and fluid accumulate in the interstitial space, causing lymphedema.3 For example, lymphedema of the arm or leg occurs after surgical removal of axillary or femoral lymph nodes, respectively, for treatment of carcinoma. Inflammation or tumours may cause lymphatic obstruction, leading to edema of the involved tissues. Clinical manifestations Edema may be localized or generalized. Localized edema is usually limited to a site of trauma, as in a sprained finger. Another kind of localized edema occurs within particular organ systems and includes cerebral, pulmonary, and laryngeal edema; pleural 373 effusion (fluid accumulation in the pleural space); pericardial effusion (fluid accumulation within the membrane around the heart); and ascites (accumulation of fluid in the peritoneal space). Edema of specific organs, such as the brain, lung, or larynx, can be life-threatening. Generalized edema is manifested by a more uniform distribution of fluid in interstitial spaces. Dependent edema, in which fluid accumulates in gravity-dependent areas of the body, might signal more generalized edema. Dependent edema appears in the feet and legs when standing and in the sacral area and buttocks when supine (lying on back). It can be identified by pressing on tissues overlying bony prominences. A pit left in the skin indicates edema (hence the term pitting edema) (Figure 5-3). FIGURE 5-3 Pitting Edema. (From Bloom, A., & Ireland, J. [1992]. Color atlas of diabetes [2nd ed.]. St. Louis: Mosby.) Edema usually is associated with weight gain, swelling and puffiness, tight-fitting clothes and shoes, limited movement of affected joints, and symptoms associated with the underlying pathological condition. Fluid accumulations increase the distance required for nutrients and waste products to move between capillaries and tissues. Blood flow may be impaired also. Therefore wounds heal more slowly, and with prolonged edema the risks of 374 infection and pressure sores over bony prominences increase. Concept of Fluid Balance and Pathophysiology As edematous fluid accumulates, it is trapped in a “third space” (i.e., the interstitial space, pleural space, pericardial space) and is unavailable for metabolic processes or perfusion. Dehydration can develop as a result of this sequestering. Such sequestration occurs with severe burns, where large amounts of vascular fluid are lost to the interstitial spaces, reducing plasma volume and causing shock (see Chapter 24). Evaluation and Treatment Specific conditions causing edema require diagnosis. Edema may be treated symptomatically until the underlying disorder is corrected. Supportive measures include elevating edematous limbs, using compression stockings, avoiding prolonged standing, restricting salt intake, and taking diuretics. Administration of intravenous (IV) albumin can be required in severe cases. Quick Check 5-1 1. How does an increase in capillary hydrostatic pressure cause edema? 2. How does a decrease in capillary oncotic pressure cause edema? Sodium, Chloride, and Water Balance The kidneys and hormones have a central role in maintaining sodium and water balance. Because water follows the osmotic gradients established by changes in salt concentration, sodium concentration and water balance are intimately related. Sodium concentration is regulated by renal effects of aldosterone (see Figure 18-18). Water balance is regulated primarily by antidiuretic hormone (ADH; also known as vasopressin). Sodium (Na+) accounts for 90% of the ECF cations (positively charged ions) (see Table 5-3). Along with its constituent anions (negatively charged ions) chloride and bicarbonate, sodium regulates extracellular osmotic forces and therefore regulates water 375 balance. Sodium is important in other functions, including maintenance of neuromuscular irritability for conduction of nerve impulses (in conjunction with potassium and calcium; see Figure 129), regulation of acid-base balance (using sodium bicarbonate and sodium phosphate), participation in cellular chemical reactions, and transport of substances across the cellular membrane. The kidney, in conjunction with neural and hormonal mediators, maintains normal serum sodium concentration within a narrow range (136 to 145 mmol/L) primarily through renal tubular reabsorption. Hormonal regulation of sodium (and potassium) balance is mediated by aldosterone, a mineralocorticoid synthesized and secreted from the adrenal cortex as a component of the renin-angiotensin-aldosterone system. Aldosterone secretion is influenced by circulating blood volume, blood pressure, and plasma concentrations of sodium and potassium. When circulating blood volume or blood pressure is reduced, sodium levels are depressed, or potassium levels are increased, renin, an enzyme secreted by the juxtaglomerular cells of the kidney, is released. Renin stimulates the formation of angiotensin I, an inactive polypeptide. Angiotensin-converting enzyme (ACE) in pulmonary vessels converts angiotensin I to angiotensin II, which stimulates the secretion of aldosterone and ADH and also causes vasoconstriction.Concept of Fluid Balance and Pathophysiology The aldosterone promotes renal sodium and water reabsorption and excretion of potassium, increasing blood volume (Figure 5-4; see also Figure 29-9). Vasoconstriction elevates the systemic blood pressure and restores renal perfusion (blood flow). This restoration inhibits the further release of renin. 376 The Renin-Angiotensin-Aldosterone System. BP, blood pressure; ECF, extracellular fluid; Na+, sodium. (Modified from Herlihy, B., & FIGURE 5-4 Maebius, N. [2011]. The human body in health and disease [4th ed.]. Philadelphia: Saunders. Borrowed from Lewis, S.L., Bucher, L., Heitkemper, M.M., et al. [2014]. Medical-surgical nursing: Assessment and management of clinical problems [9th ed.]. St. Louis: Mosby.) Natriuretic peptides are hormones primarily produced by the myocardium. Atrial natriuretic hormone (ANH) is produced by the atria. B-type natriuretic peptide (BNP) is produced by the ventricles. Urodilatin (an ANP analogue) is synthesized within the kidney. Natriuretic peptides are released when there is an increase in transmural atrial pressure (increased volume), which may occur with heart failure or when there is an increase in mean arterial pressure4 (Figure 5-5). They are natural antagonists to the reninangiotensin-aldosterone system. Natriuretic peptides cause vasodilation and increase sodium and water excretion, decreasing blood pressure. Natriuretic peptides are sometimes called a “third factor” in sodium regulation. (Increased glomerular filtration rate is thus the first factor and aldosterone the second factor.) 377 The Natriuretic Peptide System. ANH, atrial natriuretic hormone; BNP, brain natriuretic peptide; GFR, glomerular filtration rate; Na+, sodium FIGURE 5-5 Chloride (Cl?) is the major anion in ECF and provides electroneutrality, particularly in relation to sodium. Chloride transport is generally passive and follows the active transport of sodium so that increases or decreases in chloride concentration are proportional to changes in sodium concentration. Chloride concentration tends to vary inversely with changes in the concentration of bicarbonate ( ), the other major anion. Water balance is regulated by the secretion of ADH. ADH is secreted when plasma osmolality increases or circulating blood volume decreases and blood pressure drops … Get a 10 % discount on an order above $ 100 Use the following coupon code : NURSING10

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