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FLUID AND ELECTROLYTES: BALANCE AND DISTURBANCE. FLUIDS (1). 60% of adult’s weight F luid refers to water and electrolytes. F actors influencing the amount of body fluid are: A ge; young > old G ender; men > women B ody fat, thin > obese I ntracellular space Fluid in the cells,
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FLUIDS (1) • 60% of adult’s weight • Fluid refers to water and electrolytes. • Factors influencing the amount of body fluid are: • Age; young > old • Gender; men > women • Body fat, thin > obese • Intracellular space • Fluid in the cells, • Two thirds of body fluid, • Primarily in the skeletal muscle. • Extracellular space • Fluid outside the cells • Subdivides into: • Intravascular (plasma), 3 L of 6 L of blood volume. • Interstitial (surrounds the cell), 11 to 12 L adult (eg. Lymph )
FLUIDS (2) • Trans-cellular • Fluid in body spaces, 1 L, (eg. CSF, synovial, intraocular, and pleural) • Fluid shifts between two compartments to maintain equilibrium, loss of fluid disrupts equilibrium. • Sometimes, fluid is not lost from the body but is unavailable for use by either the ICF or ECF
FLUIDS (3) Third-space fluid shift, or “third spacing”. • Signs of third-space shift • Decreased urine output • Increased HR • Decreased BP • Decreased CVP • Edema • Increased body weight • Imbalance in I&O • Third-space shifts occur in the form • Ascites • Edema • Bleeding into a joint or body cavity.
ELECTROLYTES (1) • Active chemicals • Found in two forms. • Cations • carry positive charges • Sodium, Potassium, Calcium, Magnesium, and Hydrogen. • Anions, carry negative charges • Chloride, Bicarbonate, Phosphate, Sulfate, Proteinate, • Chemicals unite in varying combinations. • Concentration expressed in terms of milli-equivalents (mEq) per liter • Measure of chemical activity, rather than (mg), unit weight. • A mEq is equivalent to the electro-chemical activity of 1 mg of hydrogen. • In a solution, cations and anions are equal in mEq/L.
ELECTROLYTES (2) • Electrolyte concentrations in the ICF differ from those in the ECF • Measured in the most accessible portion of ECF (plasma) • Sodium (Na+) • The major cations in ECF • Associated with fluid volume. • Retention of Na+ associated with fluid retention, • Potassium (K+ ) • The major cation in ICF • ECF has a low concentration of K+ and tolerate small changes K+ concentrations. • Release of large stores of ICF potassium (trauma), can be extremely dangerous.
Extracellular Fluid (Plasma) Cations Sodium (Na+) 142 Potassium (K+)5 Calcium (Ca ++) 5 Magnesium (Mg ++) 2 Total cations 154 Anions Chloride (Cl- ) 103 Bicarbonate (HCO3- ) 26 Phosphate (HPO4 -) 2 Sulfate (SO4-- ) 1 Organic acids 5 Proteinate 17 Total anions 154 Intracellular Fluid Cations Potassium (K ) 150 Magnesium (Mg ) 40 Sodium (Na ) 10 Total cations 200 Anions Phosphates and sulfates 150 Bicarbonate (HCO3 ) 10 Proteinate 40 Total anions 200 ELECTROLYTES (1)
REGULATION OF FLUID • Movement of fluid through capillary walls depends on: • Hydrostatic pressure • Pressure exerted on the walls of blood vessels • Osmotic pressure • Pressure exerted by the protein in the plasma • Direction of fluid movement depends on the differences of hydrostatic and osmotic pressure • Four mechanisms work to maintain equilibrium • Osmosis • Diffusion • Filtration • Active transport
Osmosis • Movement of fluid from and area of lower solute concentration to an area of higher solute concentration
Diffusion • Movement of molecules and ions from an area of higher concentration to an area of lower concentration
Filtration • Movement of water and solutes from an area of higher hydrostatic pressure to an area of lower hydrostatic pressure
Active Transport • Physiologic pump that moves fluid from an area of lower concentration to one of higher concentration • Movement against the concentration gradient • Sodium-potassium pump maintains the higher concentration of extracellular sodium and intracellular potassium • Requires adenosine (ATP) for energy
ROUTES OF GAINS AND LOSSES • Gain • Dietary intake of fluid and food or enteral feeding • Parenteral fluids • Loss • Kidney: urine output • Skin loss: sensible and insensible losses • Lungs • GI tract • Other
Role of Atrial Natriuretic Peptide (ANP) in Maintenance of Fluid Balance
GERONTOLOGIC CONSIDERATIONS • Reduced homeostatic mechanisms: cardiac, renal, and respiratory function • Decreased body fluid percentage • Medication use • Presence of concomitant conditions
FLUID VOLUME DEFICIT (FVD) (HYPOVOLEMIA) • Occurs when loss of ECF exceeds intake. • Water and electrolytes are lost in the same proportion, so the ratio of serum electrolytes to water remains the same. • Not same a dehydration • Dehydration refers to loss of water alone with increased serum sodium levels. • FVD may occur alone or in combination with other imbalances. • Unless other imbalances are present concurrently, serum electrolyte concentrations remain essentially unchanged.
PATHOPHYSIOLOGY • Causes • Increased fluid losses: • Vomiting, Diarrhea, GI suctioning, Sweating • Decreased fluid intake • Nausea, Inability to gain access to fluids • Risk factors • Diabetes insipidus, • Adrenal insufficiency, • Osmotic diuresis, • Hemorrhage, and • Coma. • Third-space fluid shifts (eg., Burns or ascites with).
CLINICAL MANIFESTATIONS • May be mild, moderate, or severe, depending on degree of loss. • Important characteristics of FVD include: • Acute weight loss • Decreased skin turgor • Oliguria • Concentrated urine • Postural hypotension • Weak, rapid heart rate • Flattened neck veins • Increased temperature • Decreased central venous pressure • Cool, clammy skin related to peripheral vasoconstriction • Thirst • Anorexia • Nausea • Lassitude • Muscle weakness • Cramps.
ASSESSMENT AND DIAGNOSTIC FINDINGS • Health history and physical examination • Elevated BUN: creatinine ratio ( > 20:1). • BUN can be elevated due to dehydration or decreased renal perfusion and function. • Elevated hematocrit • Serum electrolyte changes may also exist. • Hypokalemia occurs with GI and renal losses. • Hyperkalemia occurs with adrenal insufficiency. • Hyponatremia occurs with increased thirst and ADH release. • Hypernatremia results from increased insensible losses and diabetes insipidus. • Urine specific gravity is increased (kidneys attempt to conserve water), and decreased with diabetes insipidus. • Urine osmolality is greater than 450 mOsm/Kg
GERONTOLOGIC CONSIDERATIONS • Physiologic changes • Reduction in total body water • Reduction in renal function (decreased ability to concentrate urine) • Decreased cardiovascular and respiratory function • Disturbances in hormonal regulatory functions. • Assessment of elderly should be modified • Skin turgor: • Less valid (skin loses elasticity) • Use other measures (eg., slowness in filling of veins) • Skin turgor is best tested over the forehead or the sternum • Functional assessment • Ability to obtain adequate intake. • Mentally status • Ambulation • Use both arms and hands • Swallow • Deliberate restriction
MEDICAL MANAGEMENT • Considers the usual maintenance requirements • Oral route (preferred) provided patient can drink, deficit not severe • IV route (when loss is acute and severe) • Isotonic solutions • Lactated Ringer ’s, 0.9% sodium chloride (normal saline) • As soon as the patient becomes normotensive, • Hypotonic solution, 0.45% sodium chloride. • Assessment • I & O, Weight, vital signs, CVP, LOC, breath sounds, skin color
If oliguria continues • Determine whether depressed renal function is due to reduced renal blood flow or to acute tubular necrosis • Do the fluid challenge test. • The goal is to provide fluids rapidly enough to attain adequate tissue perfusion without compromising the cardiovascular system. • 100 to 200 mL of normal saline solution over 15 minutes. • Monitor hemodynamic response to this treatment • vital signs, breath sounds, sensorium, central venous pressure, urine output • Response: • increased urine output, increased blood pressure, Increased central venous pressure. • Note: • Shock can occur when the volume of fluid lost exceeds 25% of the intravascular volume, or when fluid loss is rapid.
FLUID VOLUME EXCESS (FVE) (HYPERVOLEMIA) • An isotonic expansion of the ECF • Caused by the abnormal retention of water and sodium in the same proportions in which they normally exist in the ECF. • Always secondary to increased total body sodium • Leads to increased in total body water. • Serum sodium concentration remains normal.
PATHOPHYSIOLOGY • May be related to: • Simple fluid overload • Diminished function of the homeostatic mechanisms responsible for regulating fluid balance • Contributing factors • Heart failure • Renal failure • Cirrhosis of the liver. • Consumption of excessive amounts of table or other sodium salts. • Excessive administration of sodium-containing fluids in a patient with impaired regulatory mechanisms
CLINICAL MANIFESTATIONS • Edema • Distended neck veins • Crackles (abnormal lung sounds). • Tachycardia • Increased blood pressure • Increased Pulse pressure • Increased Central venous pressure • Increased weight • Increased urine output • Shortness of breath and wheezing.
ASSESSMENT AND DIAGNOSTIC FINDINGS • Decreased BUN (Plasma dilution) • Decreased hematocrit (Plasma dilution) • In chronic renal failure • Both serum osmolality and the sodium level are decreased due to excessive retention of water. • The urine sodium level is increased if the kidneys are attempting to excrete excess volume. • Chest x-rays may reveal pulmonary congestion. • Hypervolemia occurs when aldosterone is chronically stimulated (i.e., cirrhosis, heart failure, and nephrotic syndrome). • Urine sodium levels, therefore, will not rise in these conditions.
MEDICAL MANAGEMENT • Correct causes. • When FVE is related to excessive IV sodium-containing fluids (stop infusion) • Symptomatic treatment consists of: • Administering diuretics • When dietary restriction of sodium alone is insufficient • Choice of diuretic is based on: • Severity of the Hypervolemia • Degree of impairment of renal function • Potency of the diuretic • Restricting fluids and sodium.
MEDICAL MANAGEMENT (2) • Correct other electrolyte imbalances (effect of the diuretic) • Hypokalemia (Potassium supplements) • Hyperkalemia (stop diuretics, cation exchange resins) • Hyponatremia (detection, restriction of fluid) • Hypomagnesemia (stop diuretic) • Azotemia (increased nitrogen levels in the blood) can occur with FVE when urea and creatinine are not excreted due to decreased perfusion by the kidneys and decreased excretion of wastes • High uric acid levels (hyperuricemia) can also occur from increased reabsorption and decreased excretion of uric acid by the kidneys. • When renal function is impaired and drugs cannot act efficiently (hemodialysis or peritoneal dialysis) • Nutriyional therapy ( Restriction of Na intake to 250mg)
NURSING MANAGEMENT • Monitor I & O • Weight daily • Acute weight gain of 0.9 kg (about 2 lb) represents a gain of 1 L of fluid. • Breath sounds • Degree of edema in the most dependent parts of the body, • Measure circumference of the extremities • NUTRITIONAL THERAPY • Dietary restriction of sodium. • Daily average diet (normal) contains 6 to 15 g of salt • Low-sodium diets ranges from a mild restriction to 250 mg /day • Read food labels carefully to determine salt content. • Salt substitute lemon juice, onions, and garlic. • Most salt substitutes contain potassium (avoided in hyperkalemia, loop diuretics) • Salt substitutes containing ammonium chloride (avoided with liver damage) • Drinking water may contain too much sodium (Avoid water softeners that add sodium to water)
SIGNIFICANCE OF SODIUM • Most abundant caution in ECF • Serum level is 135 to 145 mEq/L • Major determinant of ECF osmolality • Regulator of ECF volume. • A loss or gain of Na+ is usually accompanied by a loss or gain of water. • Play a role in transmission of nerve impulses. • Deficit and excess are the two most common imbalances of sodium.
SODIUM DEFICIT (HYPONATREMIA) • Serum sodium level < 135 mEq/L; 135 mmol/L • Serum sodium represents the ratio of total sodium to total water of body. • Decreased ratio results from: • Low sodium with a lesser reduction in water • Normal sodium with excess water • Excess sodium with greater excess of water. • Hyponatremia state can superimposed an existing FVD or FVE. • Sodium may be lost by: • Vomiting, Diarrhea , Fistulas • Sweating • Diuretics • Low-salt diet. • A deficiency of aldosterone, as occurs in adrenal insufficiency
DILUTIONAL HYPONATREMIA • Water intoxication (dilutional hyponatremia) • Patient’s serum sodium diluted by increased volume of water • Therefore, water moves into cells, resulting in ECF volume excess. • Risk factors: • SIADH (Syndrome of Inappropriate ADH) • Hyperglycemia • Increased water intake (administration of electrolyte-poor IV fluids) • Tap-water enemas • Irrigation of nasogastric tubes with water • Excessive IV administration of dextrose and water solutions • Compulsive water drinking (psychogenic polydipsia).
SIADH • Physiology • Excessive ADH activity • Water retention • Dilutional hyponatremia • Inappropriate urinary excretion of sodium in the presence of hyponatremia. • Causes: • Sustained secretion of ADH by the hypothalamus • head injuries • endocrine and pulmonary disorders • physiologic or psychological stress • Medications • Oxytocin • Cyclophosphamide • Vincristine • Thioridazine • Amitriptyline • Production of an ADH- like substance from a tumor (aberrant ADH production). • Oat-cell lung tumors,
CLINICAL MANIFESTATIONS • Depend on the Cause, Magnitude, Speed • Manifestations • Poor skin turgor, Dry mucosa, , Decreased saliva , Orthostatic hypotention, Nausea, Abdominal cramping , • Neurologic changes • altered mental status due cellular swelling and cerebral edema • Features of hyponatremia associated with sodium loss and water gain include • Anorexia, Muscle cramps, Exhaustion • When the serum sodium level drops below 115 mEq/L (115 mmol/L) • Signs of increasing ICP • Lethargy, Confusion, Muscle twitching, Focal weakness, Hemiparesis, Papilledema, seizures
Assessment and Diagnostic Findings • Serum sodium level <135 mEq/L • In SIADH, it may reaches 100 mEq/L or less. • Serum osmolality is also decreased (except in Azotemia or ingestion of toxins) • In Azotemia, hyponatremia is due to sodium loss • Urinary sodium content is less than 20 mEq/L (20 mmol/L) • Urine specific gravity is low (1.002 to 1.004) • When hyponatremia is due to SIADH • Urinary sodium content is greater than 20 mEq/L • Urine specific gravity is usually over 1.012. • Gains body weight, but no peripheral edema fluid accumulates inside the cells. • “Fingerprinting ”
MEDICAL MANAGEMENT • SODIUM REPLACEMENT • Careful administration of sodium by Mouth, Nasogastric tube, Parenteral • For patients who can eat and drink (replacement easy, sodium is abundant in a normal diet). • For those who cannot eat, Lactated Ringer’s solution or isotonic saline (0.9% sodium chloride) • Serum sodium must not be increased by greater than 12 mEq/L in 24 hours, to avoid neurologic damage due to osmotic demyelination. • Demyelination occurs with overcorrection (above 140 mEq/L) too rapidly or in the presence of hypoxia or anoxia • It may produce lesions in the pons that cause: Paraparesis, Dysarthria, Dysphagia, Coma • Usual daily requirement in adults is 100 mEq, with no abnormal losses.
In SIADH • Hpertonic solution alone cannot change plasma sodium level. • Excess sodium would be excreted rapidly in a highly concentrated urine. • With the addition of the diuretic furosemide (Lasix), urine is not concentrated and isotonic urine is excreted to effect a change in water balance. • When water restriction is difficult, Lithium or demeclocycline • WATER RESTRICTION • Restrict fluid to 800 mL/ day • This is far safer than sodium administration • When neurologic symptoms present • Administer small volumes of a hypertonic sodium solution, such as 3% or 5% sodium chloride. • Incorrect use of these fluids is extremely dangerous • 1 L of 3% sodium chloride contains 513 mEq of sodium • 1 L of 5% sodium chloride contains 855 mEq of sodium. • If edema exists alone • Sodium is restricted • If edema and hyponatremia occur together, both sodium and water are restricted.
NURSING ALERT • Highly hypertonic sodium solutions (3% and 5% sodium chloride) should be administered only in intensive care settings under close observation • Fluids are administered slowly and in small volumes • Patient is monitored closely for fluid overload • The purpose is to relieve acute manifestations of cerebral edema and to prevent neurologic complications rather than to correct the sodium concentration • Loop diuretic to prevent ECF volume overload and to increase water excretion.
NURSING MANAGEMENT • Identify patients at risk for monitoring • Early detection and treatment to prevent serious consequences. • Monitor I & O and output and daily body weights • Note GI manifestations, such as anorexia, nausea, vomiting, and cramping • Be alert for central nervous system changes • Lethargy • Confusion • Muscle twitching • Seizures • Monitor • Serum sodium levels • Urinary sodium levels • Specific gravity • Hyponatremia is a cause of confusion in elderly • The elderly are at increased risk • Medications causing sodium loss or water retention is a predisposing factor.
DETECTING AND CONTROLLING HYPONATREMIA • Encourage foods and fluids with a high sodium content if the patient tolerates • For example, broth made with one beef cube contains approximately 900 mg of sodium; • 8 oz of tomato juice contains approximately 700 mg of sodium. • Be familiar with the sodium content of parenteral fluids • For patients taking lithium • Observe for lithium toxicity • Supplemental salt and fluid are administered • Instructed not to use diuretics without close medical supervision. • Adequate salt intake should be ensured. • Excess water supplements are avoided in patients receiving isotonic or hypotonic enteral feedings • Actual fluid needs are determined by evaluating: • Fluid intake and output • Urine specific gravity • Serum sodium levels.
NURSING ALERT • When administering fluids to patients with cardiovascular disease, the nurse assesses for signs of circulatory overload • Cough • Dyspnea • puffy eyelids • dependent edema • weight gain in 24 hours • crackles. • Extreme care is taken when administering highly hypertonic sodium (e.g., 3% or 5% sodium chloride) fluids, because these fluids can be lethal if infused carelessly. • RETURNING SODIUM LEVEL TO NORMAL • It is safer to restrict fluid intake than to administer sodium. • Administering sodium to a normo-volemia or hyper-volemia pt. causes fluid volume overload. • Monitor patients with cardiovascular disease very closely. • In severe hyponatremia, the aim of therapy is to elevate the serum sodium level only enough to alleviate neurologic signs and symptoms. • It is generally recommended that the serum sodium concentration be raised no higher than 125 mEq/L (125 mmol/L) with a hypertonic saline solution.
SODIUM EXCESS (HYPERNATREMIA) • A higher-than-normal serum sodium level (exceeding 145 mEq) • It can be caused by • Gain of sodium • Loss of water • It can occur in patients with normal fluid volume or in those with FVD or FVE. • In water loss • the patient loses more water than sodium • the kidneys attempt to conserve water • Risk factors • Fluid deprivation (unconscious, very old, very young, cognitively impaired) • Hypertonic enteral feedings without adequate water • Watery diarrhea • Increased insensible water loss (e.g., hyperventilation) • Diabetes insipidus • Deficiency of ADH • Heat stroke, near-drowning in sea water • Malfunction of either hemodialysis or peritoneal dialysis • IV administration of hypertonic saline • Excessive use of sodium bicarbonate
CLINICAL MANIFESTATIONS • Primarily neurologic (due to cellular dehydration) • Restlessness • Weakness • Disorientation • Delusions • Hallucinations • Permanent brain damage (especially in children) • Thirst (strong a defender of serum sodium levels in healthy people) • A dry, swollen tongue and sticky mucous membranes • Flushed skin • Peripheral and pulmonary edema • Postural hypotension • Increased muscle tone and deep tendon reflexes • Temperature may rise mildly
ASSESSMENT AND DIAGNOSTIC FINDINGS • Serum sodium level exceeds 145 mEq/L • Serum osmolality exceeds 295 mOsm/kg • Urine specific gravity and urine osmolality are increased
MEDICAL MANAGEMENT • Gradual lowering of serum sodium level by • Hypotonic electrolyte solution (eg,0.3% sodium chloride) • Isotonic non-saline solution (e.g., dextrose 5% in water [D5W ]) • D5W indicated (to replace water without sodium • hypotonic sodium solution to be safer than D5W (decreases the risk of cerebral edema, solution of choice in severe hyperglycemia with hypernatremia.) • Diuretics also may be prescribed to treat the sodium gain. • sodium level is reduced at a rate no faster than 0.5 to 1 mEq/L to allow sufficient time for readjustment through diffusion across fluid compartments. • Desmopressin acetate to treat diabetes insipidus
NURSING MANAGEMENT • Monitor patients at risk • Assess for abnormal losses of water or low water intake • Large gains of sodium (over-the-counter medications) • Obtain medication history • Monitor patient for thirst or elevated body temperature • Monitors changes (restlessness, disorientation, and lethargy) • Offer fluids at regular intervals • IV or enteral feeding with sufficient water • For patients with diabetes insipidus, adequate water intake • Monitor patient’s response to the fluids (serial serum sodium levels and changes in neurologic signs)
SIGNIFICANCE OF POTASSIUM • Major intracellular (98% of the body’s potassium is inside the cells • The remaining 2% is in the ECF (influence skeletal and cardiac muscles) • Normal serum level (3.5 to 5.5 mEq/L • Minor variations are significant • Imbalances are associated with many diseases, injuries, drugs (diuretics, laxatives, antibiotics) ,special treatments (TPN, chemotherapy) • 80% is excreted by kidneys (20% by bowel and in sweat) • kidneys regulate potassium balance based on the level • Aldosterone also increases the excretion of potassium by the kidney • Potassium may still be lost in urine in the presence of a potassium deficit.
POTASSIUM DEFICIT (HYPOKALEMIA) • Below-normal serum potassium level • May occur in patients with normal potassium stores (in alkalosis, a temporary shift of K+ into cells) • Risk factors • GIT losses (diarrhea, Vomiting, suction, fistulas, • Alterations in acid –base balance • Hyperaldosteronism increases renal potassium wasting • Potassium-losing diuretics, such as the thiazides (eg, chlorothiazide [Diuril] and polythiazide [Renese]) • Other drugs corticosteroids, penicillin, carbenicillin, and amphotericin B • Insulin promotes the entry of potassium into skeletal muscle and hepatic cells • Patients who are unable or unwilling to eat a normal diet (elderly people, alcoholics, anorexia nervosa) • Magnesium depletion causes renal potassium loss and must be corrected first