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Fluid, Electrolyte, and Acid-Base Imbalances.pdf

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Department
Nursing
Course
NUR 823
Professor
All Professors
Semester
Winter

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Fluid, Electrolyte, and Acid-Base Imbalances January-21-13 5:49 PM Water Content of the Body • Water accounts for 60% of adult body weight. • Varies with sex, body mass and age. ○ Lean body mass contains more water. • Infants and the elderly are at a higher risk for fluid-related problems. ○ In older adults body water content averages 45%-55%of body weight. ○ In infants, water makes up about 70-80%of total body weight. Body Fluid Compartments • Two major fluid compartmentsin the body: ○ Extracellular (outside the cells - interstitial fluid, lymph, plasma) ○ Intracellular (inside the cells, a.k.a the cytoplasm) • There is a small third compartment,known as the transcellularspace (about 1L). Includes CSF, GI tract, and pleural, synovial, and peritoneal spaces. ○ Loss of this fluid (i.e. by vomiting)can produce serious fluid and electrolyte imbalances. ○ A "third space" syndrome can occur when an increase in transcellular fluid occurs at the expense of fluid in other compartments.Examples:after intestinal paralysis, ascites, hydrocephaly or pleural or pericardial effusions. Calculation of Fluid Gain or Loss • One litre of water weighs 1kg. • Body weight change, especially sudden change, is an excellent indicator of overall volumeloss or gain. ○ Example: A person who drinks 240mLof liquid gains 0.24kg. ○ A person receiving diuretics who loses 2kg in 24 hours has lost about 2L. Electrolytes • Electrolytesare substances whose moleculesdissociate or split into ions when placed in solution. Measurement of Electrolytes • Important to the nurse in evaluating electrolytebalance, as well as determining the compositionof electrolytepreparations. ElectrolyteComposition of Fluid Compartments • Electrolytecompositionvaries between the ECF and the ICF. The overall concentration of the electrolytesis approximatelythe same in the two compartments. Mechanisms ControllingFluid and Electrolyte Movement • Diffusion is the movementof moleculesfrom an area of high concentration to an area of low concentration. ○ Net movementof molecules stops when the concentrationsare equal in both areas. • Facilitated diffusion movesmolecules from an area of high concentration to low concentration,is passive, and requires no energy other than that of the concentration gradient. ○ There must be a membrane carrier molecule to facilitate the rate of diffusion. ○ Glucose transport into the cell is an example. • Activetransport is a process requiring energy in which moleculesmoveagainst the concentrationgradient. ○ Example: the sodium-potassium pump needs ATP to be powered. • Osmosis is the movementof water between two compartmentsseparated by a membrane permeable to water but not to a solute. ○ Water moves through the membrane from an area of low solute concentration to an area of high solute concentration. Water moves from the more dilute compartment(has more water) to a more ○ Water moves from the more dilute compartment(has more water) to a more concentrated compartment(has less water). ○ Osmotic pressure is the amount of pressure required to stop the osmoticflow of water. • Hydrostatic pressure is the force within a fluid compartment.In the blood vessels, hydrostatic pressure is the blood pressure generated by the contraction of the heart. ○ Hydrostatic pressure in the vascular system gradually decreases as the blood movesthrough the arteries until it reaches about 40mmHgat the arterial end of a capillary. • Oncotic pressure (colloidal osmoticpressure) is osmoticpressure exerted by colloids in solution. ○ The major colloid in the vascular system contributing to the total osmotic pressure is protein. Protein molecules attract water, pulling fluid from the tissue space into the vascular space. ○ Unlike electrolytes,the size of protein moleculesprevent them from leaving the vascular space. Fluid Movement in Capillaries • There is normal movementof fluid between the capillary and the interstitium. The amount and direction of movementare determined by the interaction of ○ (1) capillary hydrostatic pressure ○ (2) plasma oncotic pressure ○ (3) interstitial hydrostatic pressure and ○ (4) interstitial oncotic pressure. • Capillary hydrostatic pressure and interstitial oncotic pressure cause the movementof water out of the capillaries. • Plasma oncotic pressure and interstitial hydrostatic pressure cause the movementof fluid into the capillary. • At the arterial end of a capillary, capillary hydrostatic pressure exceeds plasma oncotic pressure, and fluid is moved into the interstitium. • At the venous end of a capillary, the capillary hydrostatic pressure is lower than the plasma oncotic pressure and fluid is drawn back into the capillary by the oncotic pressure created by plasma proteins. Fluid shifts • If capillary or interstitial pressures are altered, fluid may ABNORMALLY shift from one compartmentto another, resulting in edema or dehydration. • Shifts of plasma to interstitial fluid (accumulation of fluid in the interstitium - edema): ○ Occurs if:  Venous hydrostatic pressure increases (inhibits movementback into the capillary). Examples:fluid overload, CHF, liver failure, obstruction of venous return to heart (e.g. tourniquets, restrictive clothing, venous thrombosis),and venous insufficiency (e.g. varicoseveins)  Plasma oncotic pressure decreases (fluid remains in the interstitium if plasma oncotic pressure is too low to draw fluid back into the capillary). Seen if the plasma protein content is too low. Examples: excessiveprotein loss (renal disorders), deficient protein synthesis (liver disease) and deficient protein intake (malnutrition).  Interstitial oncotic pressure rises. Trauma, burns and inflammationcan damage capillary walls and allow plasma protein to accumulate in the interstitium. • Shifts of Interstitial Fluid to Plasma. ○ Fluid is drawn into the plasma space whenever there is an increase in the plasma osmoticor oncotic pressure. ○ This could happen with the administration of colloids, dextran, mannitol, or hypertonic solutions. ○ Increasing the tissue hydrostaticpressure is another way of causing a shift of fluid into the plasma.  Example:the wearing of elastic compressionstockings or hose to  Example:the wearing of elastic compressionstockings or hose to decrease peripheral edema. Fluid Spacing • First spacing describes the normal distribution of fluid in the ICF and ECF compartments. • Second spacing refers to an abnormal accumulation of interstitial fluid (e.g. edema). • Third spacing occurs when fluid accumulatesin a portion of the body from which it is not easily exchanged with the rest of the ECF. It is trapped an essentially unavailable for functional use. E.g. ascites, sequestrationof fluid in the peritoneal cavity with peritonitis and edema associated with burns. Regulation of Water Balance Hypothalamic Regulation/PituitaryRegulation • Water balance maintained by a balance of intake and excretion. • A body fluid deficit or increase in plasma osmolalityis sensed by hypothalamic osmoreceptors,which in turn stimulate thirst and antidiuretic hormone (ADH). ○ ADH, which is stored in the anterior pituitary, stimulates water reabsorption in the renal distal and collecting tubules. • The sensitivity of the thirst mechanism decreases in older adults. • Factors that stimulateADH release include stress, increased plasma osmolality, nausea, nicotine and morphine. Adrenal Cortical Regulation • ADH affects only water reabsorption. • Hormonesreleased by the adrenal glands help regulate both water and electrolytes. • Two groups of hormonesreleased by the adrenal cortex:glucocorticoidsand mineralocorticoids. ○ Glucocorticoids(cortisol)have an ant inflammatoryeffect and increase serum glucose levels. ○ Mineralocorticoids(aldosterone)enhance sodium retention and potassium excretion.  May be triggered by decreased renal perfusion.  Kidneys respond by secreting renin into the plasma.  Angiotensin produced in the liver and normally found in blood in acted on by the renin to form angiotensin I, which converts to angiotensin II, which stimulates the adrenal cortex to secrete aldosterone. • In addition to the renin-angiotensin mechanism, increased plasma potassium, decreased plasma sodium and increased release of adrenocorticotropichormone (ACTH) from the anterior pituitary all act directly on the adrenal cortex to stimulate the secretion of aldosterone. Renal Regulation • The primary organs for regulating fluid and electrolytebalance are the kidneys. They regulate water balance through adjustments in fluid volume. • Kidneys produce about 1.5L of urine per day. Cardiac Regulation • Atrial natriuretic factor (ANF) is a hormone released by the cardiac atria in response to increased atrial pressure (increased volume). • Primary actions of ANF are vasodilation and increased urinary excretion of sodium and water, which decreases blood volume. GI Regulation • GI tract accounts for most of the water intake, but a small amount is normally eliminated from the GI tract in feces. Insensible Water Loss • Invisible vaporization from the lungs and skin • Assists in regulating body temperature. • Excessivesweating (sensible perspiration) caused by fever or high environmental temperaturescan lead to large losses of water and electrolytes. temperaturescan lead to large losses of water and electrolytes. Sodium and Volume Imbalances • Sodium plays a major role in maintaining the concentrationand the volume of the ECF. • Sodium affects the water distribution between ECF and ICF. • Sodium is also important in the generation and transmissionof nerve impulses and the regulation of acid-base balance. • The kidneys are the primary regulators of sodium balance. They regulate the ECF concentrationof sodium by excreting or retaining water under the influence of ADH. • Changes in the serum sodium level may reflect either a primary water imbalance, a primary sodium imbalance or a combination of the two. • Sodium imbalances are typically associated with imbalances in ECF volume. Hypernatremia • An elevated serum sodium may occur with water loss or sodium gain. • Na+ >145 mmol/L • Some commoncauses and clinical manifestations: Water Loss (sodium concentration) Symptoms Increased insensible water loss or perspiration d/t Intense thirst; dry, swollen high fever, heatstroke tongue Diabetes insipidus Restlessness,agitation, Osmoticdiuresis twitching Deficiency in ADH synthesis  Seizures, coma Decreasein kidney responsivenessto ADH Weakness Uncontrolled diabetes mellitus Postural hypotension Weight loss Sodium Gain Symptoms IV hypertonic NaCl Restlessness,agitation, IV sodium bicarbonate twitching IV excessiveisotonic NaCl Seizures, coma Primary hyperaldosteronism(hypersecretionof Flushed skin aldosterone) Weight gain Saltwater near-drowning (ingestion of seawater) Peripheral and pulmonary Administration of concentrated hyperosmolartube edema feedings Increased BP Intense thirst • Because sodium is the major determinant of the ECF osmolality,hypernatremia causes hyperosmolality.In turn, hyperosmolalitycauses a shift of water out of the cells, which leads to cellular dehydration. • The primary protectionagainst hyperosmolalityis thirst. • Hypernatremia is not a problem in an alert person who has access to water, can sense thirst, and is able to swallow. • Treatment: ○ Goal is to treat underlying cause ○ In primary water deficit, the continued water loss must be prevented and water replacementmust be provided. ○ Goal of treatmentfor NaCl excess is to dilute the sodium concentrationwith salt-free IV fluids, such as 5% dextrose in water and to promoteexcretionof the excess sodium by diuretics. Sodium intake will also be restricted. Hyponatremia • May result from loss of sodium-containing fluids or from water excess. • Na+ <135 mmol/L • Causes hypo-osmolalotywith a shift of water into the cells. Sodium Loss Symptoms GI Losses: diarrhea, vomiting, fistulas, NG suctionIrritability, apprehension, confusion Renal losses: diuretics, adrenal insufficiency, Na+Postural hypotension Renal losses: diuretics, adrenal insufficiency, Na+ Postural hypotension wasting renal disease Tachycardia Skin losses: burns, wound drainage Rapid, thready pulse Decreased jugular venous filling Nausea, vomiting Dry mucous membranes Weight loss Tremors,seizures, coma Water Gain (Sodium Dilution) Symptoms CHF Nausea, vomiting Excessivehypotonic IV fluids Weight gain Primary poluydipsia Increased BP Muscle spasms, seizures, coma Headache, lassitude, apathy, weakness, confusion • Symptomsof hyponatremiaare related to cellular swelling and are first manifested in the CNS. The excess water lowers plasma osmoalality,shifting fluid into brain cells. ExtracellularFluid Volume Imbalances • ECF volume deficit (hypovolemia) • ECF volume excess (hypervolemia) are commonlyoccurring clinical conditions. • ECF volume imbalances are typically accompanied by one or more electrolyte imbalances. Potassium Imbalances • Major ICF cation, with 98% of body potassium being intracellular. • Serum (ECF) levels are 3.5-5.0 mmol/L; intracellular concentrationsare 140-150 mmol/L. • Many of the symptomsrelated to potassium imbalance are due to changes in the ratio of ECF to ICF potassium. • Potassium is critical for many cellular and metabolic functions. ○ Necessary for the transmission and conduction of nerve impulses ○ Maintenance of normal cardiac rhythms ○ Skeletal and smooth muscle contraction ○ As the major intracellular cation, K+ regulates intracellular osmolalityand promotescellular growth. ○ Plays a role in acid-base balance. • Diet is the source of potassium. • Kidneys are primary route for potassium loss. About 90% of daily potassium intake is regulated by the kidneys, the remainder is lost in stool and sweat. ○ If kidney function is significantly impaired, toxic levels of potassium may be retained. ○ There is an inverse relationship between sodium and potassium loss. Factors that promotesodium retention (i.e. increased aldosterone),promotepotassium loss. ○ Large urine volumescan be associated with excess loss of potassium. • Disruptions between ICF and ECF potassium often cause clinical problems. • Factors causing K+ to movefrom the ECF to the ICF: ○ Insulin ○ Alkalosis ○ B-Andregenic stimulation (catecholaminerelease in stress, coronaryischemia, delirium tremens, administration of B-andregenic agonist drugs) ○ Rapid cell building (administrationof folic acid or vitamin B12 to someonewith megaloblasticanemia, resulting in marked production of RBCs) • Factors that cause K+ to movefrom ICF to ECF include: ○ Acidosis ○ Trauma to cells Exercise ○ Exercise Hyperkalemia • Hyperkalemiais high serum potassium (>5.0 mmol/L). • Causes: ○ May be caused by massive intake of potassium, impaired renal excretion, shift of potassium from ICF to ECF, or a combination. ○ Most commoncause of hyperkalemiais renal failure. ○ Also commonin clients with massive cell destruction (e.g. burn or crush injury, tumour lysis), rapid transfusion of aged blood and catabolic state (e.g. severe sepsis). ○ Metabolic acidosis, particularly when chloride is normal, is associated with a shift of potassium ions from ICF to ECF as hydrogen ions move into the cell. ○ Adrenal insufficiency leads to retention of K+ in the serum because of aldosteronedeficiency (because aldosterone conservessodium and excretes potassium). ○ Certain drugs such as K+-sparing diuretics and ACE inhibitors may contribute to the developmentof hyperkalemia. • Manifestations: ○ Ca
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