Fluids & Electrolytes

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Fluids in Human Body I. Fluid Status of Human Body A. Homeostasis: state of the body when maintaining a state of balance in the presence of constantly changing conditions B. Includes balance of fluid, electrolytes, and acid-base balance C. Body water intake and output approximately equal (2500 mL/24 hr.) II. Body Fluid Composition A. Water: 60% of body weight B. Electrolytes: substances that become charged particles in solution 1. Cations: positively charged (e.g. Na+, K+) 2. Anions: negatively charged (e.g. Cl-) 3. Both are measured in milliequivalents per liter (mEq/L) C. Osmolality: concentration of a solution measured in milliosmoles per liter D. Balance of hydrostatic pressure and osmotic pressure regulates movement of water between intravascular and interstitial spaces III. Body Fluid Distribution: A. 2 body compartments: 1. Intracellular fluids (ICF): fluids within cells of body [major intracellular electrolytes: Potassium (K+), Magnesium (Mg +2)] 2. Extracellular fluids (ECF): fluid outside cells; [major extracellular electrolytes: Sodium (Na+), Chloride(Cl-)]; this is where transportation of nutrients, oxygen, and waste products occurs B. Locations of ECF: 1. Interstitial: fluid between most cells

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2. Intravascular: fluid within blood vessels; also called plasma 3. Transcellular: fluids of body including urine, digestive secretion, cerebrospinal, pleural, synovial, intraocular, gonadal, pericardial IV. Mechanisms of Body Fluid Movement (i.e. movement of solutes, solvents across different extracellular locations) A. Osmosis: water is mover; water moves from lower concentration to higher concentration 1. Normal Osmolality of ICF and ECF: 275 – 295 mOsm/kg 2. Types of solutions according to osmolality a. Isotonic: all solutions with osmolality same as that of plasma Body cells placed in isotonic fluid: neither shrink nor swell b. Hypertonic: fluid with greater concentration of solutes than plasma Cells in hypertonic solution: water in cells moves to outside to equalize concentrations: cells will shrink c. Hypotonic: fluid with lower concentration of solutes than plasma Cells in hypotonic solution: water outside cells moves to inside of cells: cells will swell and eventually burst (hemolyze) 3. Different intravenous solutions, used to correct some abnormal conditions, categorized according to osmolality: a. Hypertonic: 5%glucose ,45% NaCl solution b. Isotonic: 9% NaCl, Lactated Ringers solution c. Hypotonic: 45% NaCl B. Diffusion: solute molecules move from higher concentration to lower concentration

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1. Solute, such as electrolytes, is the mover; not the water 2. Types: simple and facilitated (movement of large water-soluble molecules) C. Filtration: water and solutes move from area of higher hydrostatic pressure to lower hydrostatic pressure 1. Hydrostatic pressure is created by pumping action of heart and gravity against capillary wall 2. Usually occurs across capillary membranes D. Active Transport: molecules move across cell membranes against concentration gradient; requires energy, e.g. Na – K pump V. Mechanisms that Regulate Homeostasis: How the body adapts to fluid and electrolyte changes A. Thirst: primary regulator of water intake (thirst center in brain) B. Kidneys: regulator of volume and osmolality by controlling excretion of water and electrolytes C. Renin-angiotension-aldosterone mechanism: response to a drop in blood pressure; results from vasoconstriction and sodium regulation by aldosterone D. Antidiuretic hormone: hormone to regulate water excretion; responds to osmolality and blood volume E. Atrial natriuretic factor: hormone from atrial heart muscle in response to fluid excess; causes increased urine output by blocking aldosterone

Fluid and Electrolyte Imbalances I. Fluid Volume Deficit (too little fluid in body) A. Common Stimuli:

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1. Excessive fluid loss, e.g. hemorrhage, excess loss of GI fluids (vomiting, diarrhea, or wound drainage) 2. Insufficient fluid intake, e.g. no access to fluid, unable to drink 3. Failure of regulatory mechanisms, fluid shifts B. Terminology: 1. Dehydration: technically loss of water alone (but usually any state of low fluid) 2. Hypovolemia: decreased circulating blood volume 3. Third Spacing: shift of fluid from vascular space (inside blood vessels) to another area such as abdomen/bowels, soft tissues (like swelling that occurs with a severe injury –like a twisted ankle) C. Signs/Symptoms More rapid fluid loss, equals more rapid development of symptoms 1. Weight loss (liter fluid = 2.2 lb or 1 kg.) 2. Diminished skin turgor, tongue turgor (more reliable in elderly) 3. Postural (orthostatic) hypotension: drop of 15mm Hg of systolic BP with position change from lying to standing 4. Flat neck veins when recumbent 5. Diagnostic test findings (usual, not absolute): a. Electrolytes: isotonic fluid loss: Na is within normal limits; if loss of water only, Na is elevated

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b. Serum Osmolality: isotonic fluid loss: osmolality is within normal limits; loss of water alone, osmolality is elevated c. Urine specific gravity, urine osmolality: both elevated as urine becomes more concentrated as kidneys conserve water d. Increased hematocrit due to hemoconcentration e. Possible elevated blood urea nitrogen (BUN) f. CVP (mean pressure in right atrium of heart) sub normal D. Compensatory Mechanisms (how the body responds to restore homeostasis) Goal: to conserve water and Na; to maintain circulation 1. Tachycardia (may lead to hypotension) 2. Vasoconstriction as evidenced by pale, cool skin 3. Decrease in urinary output with rise in urine specific gravity E. Collaborative Care 1. Prevent deficits in clients at risk: especially aged; anyone with increased fluid loss, such as persons with prolonged vomiting and diarrhea; during hot weather, those under physical exertion without adequate fluid replacement 2. Correct the deficits and treat the underlying cause a. Replacement of fluids and electrolytes by oral, IV, or enteral route; Isotonic

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electrolyte IV solutions for hypotensive clients and those with abnormal losses b. Fluid challenge: Physician orders a specific amount of IV fluid over short period of time (e.g. 300 mL of isotonic solution over 10 minutes). Obtain baseline assessment of vital signs, breath sounds, output, mental status before initiation; compare results after fluid challenge completed; physician re-evaluates response and orders fluids accordingly c. Assess parameters pertinent to the signs and symptoms, vital signs, and level of consciousness; reassess lab results d. Notify physician if urine output < 30 mL/hr (client has a foley catheter with hourly output as monitoring) 3. Pertinent nursing diagnoses a. Deficit Fluid Volume b. Ineffective Tissue Perfusion c. Risk for Injury II.Fluid Volume Excess (too much fluid in body) Water and sodium are proportionately excessive and in extracellular compartment A.Common Stimuli (one or combinations of conditions) 1. Pathophysiology: mechanisms that should maintain homeostasis are impaired: a. Heart failure b. Kidney failure

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c. Cirrhosis of liver d. Adrenal disorders or corticosteroid administration e. Stress conditions causing release of ADH and aldosterone 2. Excessive intake of sodium and fluid a. Excessive intake of foods high in sodium (salt) b. Excessive intake of IV fluids containing sodium (0.09% NaCl) B.Terminology 1. Hypervolemia: excess intravascular fluid 2. Edema: excess interstitial fluid C.Signs/Symptoms 1. Weight gain: > 5% of body weight over short time 2. Circulatory overload: bounding pulse; S3 heart sound; neck and peripheral vein distention; increased CVP, i.e. mean pressure in right atrium of heart; cough; dyspnea; orthopnea; breath sounds, moist crackles; pulmonary edema; polyuria; ascites 3. Peripheral edema worse in most dependent body part: pedal, sacral for bed-bound client; anasarca (severe generalized over all body edema); possibly cerebral edema, i.e. altered mental status 4. Diagnostic test findings: a. Chest xray: variable degrees of pulmonary edema

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b. Serum sodium and osmolality: usually within normal range c. Hematocrit and hemoglobin: usually slightly decreased d. Decreased blood urea nitrogen (BUN), in some cases D.Compensatory Mechanisms Heart failure results when heart is unable to increase workload to handle excess blood volume 1. Left-side heart failure: pulmonary edema 2. Right-side heart failure: peripheral edema E. Collaborative Care 1. Prevent fluid volume excess in at risk populations (those receiving IV fluids, significant at risk health histories, elderly) 2. Effective fluid management: a. Assessment of signs/symptoms of fluid overload, lab results b. Fluid restrictions as ordered c. Dietary management: sodium-restricted diets d. Monitor intake and output, daily weights 3. Treatment with diuretic medications a. Loop diuretics (e.g. Furosemide (Lasix)) b. Thiazide-type diuretics (e.g. Hydrochlorothiazide (HCTZ)) c. Potassium-sparing diuretics (e.g. Bumetanide (Bumex)) F. Nursing Diagnoses 1. Excess Fluid Volume

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2. Risk for Impaired Skin Integrity (related to peripheral edema) 3. Risk for Impaired Gas Exchange (related to pulmonary congestion and/or edema) 4. Activity Intolerance III. Electrolyte Imbalances One electrolyte or several; often treat underlying cause; careful observation as over treatment may cause additional imbalances A. Sodium 1. Characteristics: a. Mainly in ECF b. Blood normal values: 135 – 145 mEq/L c. Actions: 1. Regulates volume 2. Regulates osmolality 3. Maintains neuromuscular activity d. Sources: dietary intake, prescription drugs and self-remedies e. Compensatory mechanisms: kidney excretes or conserves sodium in response to changes in vascular volume, e.g. drop in blood pressure 1. Stimulates renin-angiotensionaldosterone system 2. Regulates ADH secretion 3. Modulates glomerular filtration rate 4. Controls Atrial natriuretic peptide release (sodium excretion) 2. Hyponatremia

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Serum sodium is lower than normal (Serum Na < 135 mEq/L) a. Common Stimuli 1. Water shifts to ECF; osmolality changes and cells swell 2. Loss of sodium (without water) a. Excessive through urine (e.g.diuretics, kidney disease) b. GI (e.g. vomiting, diarrhea, GI suction) c. Skin (e.g. sweating, burns) d. Water gain to dilute ECF 3. Diseases: heart or renal failure; cirrhosis; Syndrome of Inappropriate secretion of Anti-Diuretic Hormone (SIADH); excessive hypotonic IV fluids b. Signs and Symptoms (depend on rapidity and severity of onset) 1. Early: (Na at 125) a. Muscle cramps, weakness, fatigue b. GI: anorexia, vomiting, diarrhea, nausea, abdominal cramping 2. Later (Na<120) a. Cerebral edema symptoms (brain cells swell) b. Headache, depression, personality changes

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c. Lethargy, muscle twitching, tremors d. Further progress to convulsions and coma with severely low levels 3. Diagnostic test findings a. Decreased serum Na (<135 mEq/L) b. Serum Osmolality (<275 mOsm/kg) c. 24-hour urine collection for Na used to differentiate cause c. Collaborative Care Restoration of blood volume and sodium levels 1. Medications a. Isotonic IV solution (Ringer’s, 0.9% NaCl) b. Hypertonic IV Na solution (3% NaCl) is used to treat the client with severe hyponatremia (Na : 110 – 115 mEq/L) c. Loop diuretics (e.g. Furosemide) to promote isotonic diuresis 2. Fluid and Dietary Management a. Increase foods high in sodium b. Restrict fluid in volume 3. Assessment of signs/symptoms of hyponatremia, especially

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a. Continual mental status assessment b. Seizure precautions c. Strict intake and output and monitoring weight daily d. Reassess lab results d. Nursing Diagnoses 1. Risk for Impaired Fluid Volume 2. Risk for Decreased Intracranial Adaptive Capacity 3. Hypernatremia Serum sodium is higher than normal (Serum sodium>145 mEq/L) Hyperosmolality of ECF; may occur with fluid volume deficit or excess a. Common Stimuli 1. Sodium gained in excess of water, e.g. excessive salt intake or hypertonic IV solutions, clients with heat stroke, near drowning in seawater 2. Water lost in excess of sodium, e.g. clients unable to respond to thirst as with altered mental status or physical disability; diabetes insipidus b. Signs and Symptoms (depend on rapidity and severity of onset) 1. Initially: thirst 2. If not responded to: altered neurologic function; lethargy; irritability; seizures; coma; death

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3. Diagnostic test findings: a. Serum Na is greater than 145 mEq/L b. Serum Osmolality > 295 mOsm/kg c. Collaborative Care 1. Treatment according to cause with slow correction of Na to avoid development of cerebral edema 2. Medications a. Oral or intravenous water replacement (hypotonic IV solutions such as 5%dextrose or 0.45% NaCl) b. Diuretics for Na excretion 3. Assessment a. Nursing history for precipitating factors as stimuli b. Vital signs, including temperature c. Mental status d. Signs/symptoms consistent with fluid volume deficit or excess e. Reassess lab results d. Nursing Diagnoses: Risk for Injury B. Potassium 1. Characteristics a. Primary intracellular cation

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b. Normal serum potassium level 3.5 – 5.0 mEq/L c. Actions: vital role in cellular metabolism, heart function, and neuromuscular function d. Need daily intake of potassium, usually through food e. Kidneys eliminate potassium from body under regulation by aldosterone f. Shifts in and out of cells in response to concentration of hydrogen ion (pH) in the blood 2. Hypokalemia Serum potassium is lower than normal (< 3.5 mEq/L) a. Common Stimuli 1. Excessive loss of potassium a. Through kidneys: secondary to drugs, hyperaldosteronism, diabetes mellitus b. Through GI tract: severe vomiting, gastric suction, diarrhea or ileostomy drainage 2. Inadequate intake a. Unable or unwilling to eat, anorexia nervosa b. Alcoholism 3. Shift from extracellular to intracellular space b. Signs and Symptoms

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1. Abnormal heart rhythms including atrial and ventricular Potentiates digitalis toxicity (medication to treat heart failure) 2. Muscle weakness, including leg cramps 3. Slowed abdominal peristalsis 4. Diagnostic test findings: a. Serum K: if K+=2.5 – 3.0, moderate; if < 2.5, severe and probably symptomatic b. Arterial blood gases (hypokalemia associated with alkalosis, elevated pH) c. Electrocardiogram changes: flattened or inverted T, U waves c. Collaborative Care 1. Medications a. Potassium supplements, oral or parenteral b. Never give potassium IV push, only as IV infusion 2. Dietary management Potassium rich foods (fruits and vegetables) 3. Health promotion: Prevention of hypokalemia a. Using balanced electrolyte fluids with GI loss

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b. Diet teaching and/or potassium supplements with meds that predispose to hypokalemia c. Regular monitoring of serum potassium levels 4. Assessment a. Nursing history for precipitating factors as stimuli b. Mental status c. Vital signs d. Reassess lab results d. Nursing Diagnoses 1. Activity Intolerance 2. Decreased Cardiac Output 3. Risk for Imbalance Fluid Volume 4. Acute Pain (Potassium can be irritating to veins even when diluted; never give IV push) 3. Hyperkalemia Serum potassium is higher than normal (>5.0 mEq/L) a. Common Stimuli 1. Inadequate excretion of potassium a. Impaired renal excretion of potassium (untreated renal failure, adrenal insufficiency) b. Medications that impair K+ excretion by kidneys (e.g. K+ sparing diuretics) 2. Excessively high intake of potassium

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a. Excess oral potassium by supplement, salt-substitute b. Rapid IV administration of potassium, transfusion of aged blood 3. Shift from intracellular to extracellular space May occur with acidosis, severe tissue trauma b. Signs and Symptoms 1. Abnormal heart function: slowing of heart rate and conduction; ventricular dysrhythmias progress to cardiac arrest 2. Skeletal muscle irritability, tremors progress to weakness, and paralysis 3. GI disturbances: initially, diarrhea and colic 4. Diagnostic test findings a. Serum K: > 5.0 mEq/L b. Electrocardiogram: peaked T waves, prolonged conduction PR, QRS c. Arterial blood gases to determine presence of acidosis c. Collaborative Care 1. Medications a. Stop all potassium supplements orally and IV, if receiving b. Medications to lower serum potassium and stabilize

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conduction system of heart, including 1. Intravenous Calcium Gluconate 2. Intravenous 50 gm of glucose and regular insulin (Moves K+ intracellularly) 3. Sodium polystyrene sulfonate (Kayexalate), orally or rectally (binds K+ in GI tract) c. Loop diuretics (e.g. Furosemide (Lasix)), if adequate renal function 2. Dialysis “artificial kidney” removes excess potassium 3. Health promotion: Teach clients at risk to read food and dietary supplements for potassium 4. Assessment a. Nursing history for precipitating factors as stimuli b. Cardiac status with continuous cardiac monitoring c. Vital signs d. Reassess lab results. e. Hemolyzed blood sample: if serum K+ is very high and client does not appear ill enough to have a potassium that high, blood should be redrawn and re-

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tested. First blood sample may have been hemolyzed. d. Nursing Diagnoses 1. Risk for Activity Intolerance 2. Risk for Decreased Cardiac Output 3. Risk for Imbalanced Fluid Volume C. Calcium 1. Characteristics a. Abundant in body b. Normal serum calcium level 8.5 – 10.0 mEq/L c. Body’s source is from diet; 20% of calcium ingested is absorbed d. 99% calcium is in bones and teeth and is bound to phosphorus e. Extracellular, and only ionized form is active f. Actions: 1. Regulates muscle contraction and relaxation, including respiratory muscles 2. Maintains cardiac function 3. Acts in blood clotting process g. Calcium levels are affected by acid-base balance 2. Hypocalcemia Total serum calcium level < 8.5 mg/dL Systemic effects caused by decreased levels of ionized Ca in extracellular fluid a. Common Stimuli

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1. Hypoparathyroidism (neck surgery 24 – 48 hr post op) 2. Acute pancreatitis 3. Electrolyte imbalances (low magnesium, high phosphate), alkalosis 4. Malabsorption disorders 5. Certain medications, e.g. loop diuretics (Furosemide) anticonvulsants (phenytoin (Dilantin)) 6. Massive transfusion of banked blood b. Signs and Symptoms 1. Neuromuscular: a. Most serious is tetany (tonic muscle spasm) and convulsions b. Earlier: numbness and tingling around mouth, in hands and feet advancing to muscle spasms of face and extremities, hyperactive deep tendon reflexes (DTR’s) c. Positive Chvostek’s sign: face spasm with cheek tapping; positive Trousseau’s sign: carpal spasm with inflation of BP cuff on arm 2. Respiratory status: muscle spasms can lead to laryngeal spasms

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3. Cardiac: hypotension, bradycardia, ventricular dysrhythmias and cardiac arrest 4. Diagnostic test findings a. Total serum Ca < 8.5 mg/dL b. Serum albumin affects Ca c. Serum magnesium: low, < 1.6 mg/dL is associated with low Ca d. Serum phosphate: elevated, > 4.5 mg/dL is inversely related to Ca e. Parathryoid hormone (PTH) to detect hyperparathyroidism f. Electrocardiogram: evaluate cardiac conduction: such as prolonged ST segment c. Collaborative Care 1. Medications a. Calcium supplements: b. Severe hypocalcemia: intravenous (CaChloride or CaGluconate) c. Chronic asymptomatic; oral forms, sometimes with Vitamin D 2. Dietary management includes calcium in diet (milk, figs, salmon) 3. Health promotion: Teaching to include prevention of osteoporosis

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(calcium moves from bones; not measured by serum Ca) 4. Assessment: a. Nursing history for precipitating factors as stimuli b. Neuro assessment, cardiac status and vital signs c. Continuous cardiac monitoring and airway support, if indicated; d. Reassess lab results d. Nursing Diagnoses: Risk for Injury 3. Hypercalcemia Total serum calcium level > 10.0 mg/dL. Systemic effects caused by increased levels of ionized Ca in extracellular fluid a. Common Stimuli 1. Increased reabsorption of calcium from bones a. Hyperparathyroidism b. Malignancies: cancers with metastasis (bone destruction by the tumor) c. Result of immobility and lack of weight-bearing 2. Diminished elimination of calcium Occurs with medications (e.g. thiazide diuretics, lithium) b. Signs and Symptoms 1. Decreased neuromuscular irritability: muscle weakness, depressed deep

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tendon reflexes (DTR), advances to confusion, lethargy to coma 2. GI: anorexia, nausea, vomiting, constipation 3. Cardiac: heart conduction disturbances: bradycardia, heart block 4. Polyuria and increased thirst 5. Complications: peptic ulcer disease, pancreatitis, renal calculi (kidney stones) 6. Hypercalcemic crisis; acute Ca excess, can lead to cardiac arrest 7. Diagnostic test findings a. Serum calcium >10.0 mg/dL b. Serum Parathyroid level c. Electrocardiogram: changes including shortened QT, bradycardia, heart blocks c. Collaborative Care Goal: to promote Ca elimination by kidneys; to reduce Ca reabsorption from bone 1. Medications a. Intravenous fluids: usually isotonic saline b. Loop diuretic (e.g. Furosemide (Lasix) Calcitonin) c. For hypercalcemic crisis: IV sodium phosphate or potassium phosphate

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d. For inhibiting bone reabsorption: Plicamycin (Mithracin) e. Glucocorticoids 2. Dietary Management: Increase intake of acid ash foods, fiber, fluid intake 3. Health Promotion a. Identify persons at risk b. Encourage weight-bearing activity c. Fluids up to 3 -4 quarts, if not contraindicated d. Limit calcium foods and supplements and calcium containing antacids 4. Assessment a. Nursing history for precipitating factors as stimuli b. Vital signs c. Neuro assessment d. Cardiac status, continuous cardiac monitoring if indicated e. Reassess lab results (increased risk for digitalis toxicity) d. Nursing Diagnoses 1. Risk for Injury 2. Risk for Excess Fluid Volume D.Magnesium 1. Characteristics a. Mainly intracellular and in bone

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b. Normal serum level 1.6 – 2.6 mg/dL c. Obtained through diet (green vegetables, meat, grains, nuts) d. Excreted by kidneys e. Vital to cellular processes, enzyme, protein synthesis f. Sedative effect on neuromuscular junction g. Affected by potassium and calcium levels 2. Hypomagnesemia Magnesium level < 1.6 mg/dL Common in critically ill patients a. Common stimuli 1. Usually occurs along with K and Ca deficiencies 2. Loss of GI fluids as with diarrhea, ileostomy 3. Impaired nutrition absorption from gut; starvation, NPO status 4. Chronic alcoholism 5. Medications such as loop or thiazide diuretics, some antibiotics b. Signs and Symptoms 1. Increased neuromuscular excitability: tremors, hyperactive reflexes, tetany, mood changes 2. Cardiac: dysrhythmias and sudden death; increased risk of digitalis toxicity 3. GI: nausea, vomiting, diarrhea, anorexia, abdominal distention 4. Diagnostic test findings:

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a. Electrolyte levels; low magnesium often with low Ca and K b.Electrocardiogram: delayed conduction with dysrhythmias, cardiac arrest, sudden death c. Collaborative Care 1. Medications: if symptomatic, treated with IV Magnesium Sulfate, and/or oral supplements 2. Dietary Management: encourage balanced diet including green vegetables, meat, grains, nuts, seafood 3. Health Promotion a. Identify persons at risk (postsurgery clients, clients with malnutrition, alcoholics) b. Encourage well-balanced nutrition 4. Assessment a. Nursing history for precipitating factors as stimuli b. Vital signs c. Neuro status d. Cardiac status, continuous cardiac monitoring e. GI assessment f. Reassess lab results (increased risk for digitalis toxicity) d. Nursing Diagnoses: Risk for Injury

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3. Hypermagnesemia Magnesium level >2.6 mg/dL Less common a. Common Stimuli: renal failure, especially clients receiving parenteral or oral supplements b. Signs and Symptoms 1. Neuromuscular: weakness, lethargy leading to weak or absent deep tendon reflexes (DTR), drowsiness as level rises 2. Cardiovascular: hypotension, flushing, sweating, bradydysrhytmias leading to heart block, cardiac arrest as level rises; respiratory depression with high levels 3. GI: nausea and vomiting 4. Diagnostic test findings a. Magnesium level elevated b. Electorcardiogram: changes with bradycardia, heart block c. Collaborative Care 1. Medications a. Withhold medications containing magnesium b. Dialysis for clients with renal failure c. Calcium Gluconate IV for reversal or neuro and cardiac effects

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2. Health Promotion a. Identify clients at risk (those with renal failure, receiving magnesium supplements) b. Teach to avoid laxatives, antacids, and enemas containing magnesium 3. Assessment a. Nursing history for precipitating factors as stimuli b. Neuromuscular assessment c. Cardiac assessment, continuous cardiac monitoring and airway support if indicated d. Reassess lab results d. Nursing Diagnoses 1. Decreased Cardiac Output 2. Risk for Ineffective Breathing Pattern 3. Risk for Injury E. Phosphate 1. Characteristics a. Mostly in bone; intracellular anion b. Normal serum level 2.5 – 4.5 mg/dL c. Essential to intracellular processes, including muscle contraction and nerve conduction, metabolism, acid base balance d. Source is from diet, excreted by kidneys e. Inverse relationship with calcium 2. Hypophosphatemia

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Serum phosphorus < 2.5 mg/dL Total body deficit or cellular shift a. Common Stimuli 1. Usually iatrogenic (related to treatment) 2. Refeeding syndrome: occurs with beginning enteral or total parenteral feedings to malnourished clients 3. Medications: intravenous glucose solutions, diuretics, aluminum or magnesium-based antacids 4. Alcoholism 5. Hyperventilation with respiratory alkalosis b. Signs and Symptoms 1. Neuromuscular: irritability, weakness, paresthesias, confusion, and seizures leading to respiratory failure 2. Cardiac: dysrhythmias, chest pain 3. GI: anorexia, dysphagia, nausea, vomiting, decreased GI motility 4. Diagnostic test findings: serum phosphate is <2.5 mg/dL c. Collaborative Care 1. Medications a. Oral phosphate supplements (Neutra-Phos) b. Intravenous phosphorus such as Na Phosphate, K Phosphate

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c. Eliminate phosphate depleting medications, if possible 2. Dietary Management: stress wellbalanced diet 3. Health Promotion a. Identify clients at risk b. Teach, including avoidance of phosphorus-binding antacids 4. Assessment a. Nursing history for precipitating factors as stimuli b. Neuromuscular c. GI d. Cardiac with cardiac monitoring and respiratory support if indicated e. Reassess lab results, especially electrolytes d. Nursing Diagnoses 1. Impaired Physical Mobility 2. Ineffective Breathing Pattern 3. Decreased Cardiac Output 4. Risk for Injury 3. Hyperphosphatemia Serum phosphorus > 4.5 mg/dL Impaired excretion, total body excess or cellular shift a. Common Stimuli 1. Acute or chronic renal failure 2. Excess or rapid intake of phosphates

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3. Phosphate shifts from chemotherapy, trauma, heat stroke 4. Accompanies altered calcium concentrations b. Signs and Symptoms 1. Neuromuscular: muscle cramps, paresthesias, muscle spasms, tetany 2. Calcification of soft tissues 3. Diagnostic test findings: serum phosphate is >4.5 mg/d/L c. Collaborative Care 1. Treat cause 2. Promote renal excretion by IV saline or dialysis for client in renal failure 3. Dietary Management: eliminate phosphate rich foods, such as organ meats, milk, and milk products 4. Health Promotion a. Identify clients at risk b. Teach, including avoidance of phosphate sources, foods or medications 5. Assessment a. Nursing history for precipitating factors as stimuli b. Neuromuscular c. Reassess lab results, especially electrolytes d. Nursing Diagnoses: Risk for Injury

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Acid-Base Balance I. Background A. Facts and Definitions 1. Acid-base homeostasis is necessary to maintain life. 2. Acid base balance must be within a definite range for cellular function to occur. 3. The acidity of a substance, determined by the hydrogen ion (H+) concentration; is expressed as pH. 4. Acids a. Release hydrogen ions into solution b. Have pH < 7 5. Alkalines (bases) a. Accept hydrogen ions into solution b. Have pH > 7 B. Body fluids 1. Normally slightly alkaline 2. Normal range is narrow: 7.35 – 7.45 (pH of 7 is neutral) 3. Arterial blood pH < 7.35 is considered acid 4. Arterial blood pH > 7.45 is considered alkaline : C. Acids and Bases in the body 1. Body functions constantly produce acids 2. Most acids and bases in the body are weak 3. Acids include a. Carbonic acid, which is eliminated as a gas, carbon dioxide b. Lactic, hydrochloric, phosphoric, sulfuric acids, which are metabolized or excreted as fluids 4. Bicarbonate is the major base II. Body regulation of acid-base balance

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Constant response to changes in pH to maintain the pH in the normal range 3 systems in the body, with various response times, to maintain acid-base balance :

A. Buffer System 1. Responds immediately, but has limited capacity to maintain 2. Buffers: substances that bind or release hydrogen ions a. When body fluid becomes acid, buffers bind with hydrogen ions to raise pH b. When body fluid becomes alkaline, buffers release hydrogen ions to lower pH 3. Buffer systems a. Bicarbonate-carbonic acid buffer system CO2 + H20

H2C03  H+ + HC03 weak acid

weak base

Process is reversible but the ratio of 20 (bicarbonate) to 1 (hydrogen) must be maintained b. Protein buffer system (intracellular and plasma) c. Phosphates buffer system B. Respiratory System 1. Responds within minutes 2. Includes respiratory center of brain stem and lungs 3. Occurs automatically, not under voluntary control 4. Adjusts the depth and frequency of respiration according to the pH of the blood; increases or decreases the amount of carbon dioxide in the blood;

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controls the amount of carbonic acid formed and adjusts the pH of the blood a. Hyperventilation: increased depth and frequency of respiration; blows off more CO2 in response to an acid pH b. Hypoventilation: decreased depth and frequency of respiration; retains more CO2 in response to an alkaline pH C. Renal (Metabolic) System 1. Responds within hours to days 2. Adjusts the amounts of hydrogen and bicarbonate ions a. Kidneys excrete H+ ions, or generate and reabsorb bicarbonate ions, in response to an acid pH b. Kidneys retain H+ ions, or generate and excrete bicarbonate ions, in response to an alkaline pH III. Determination of Acid-Base Balance: Analysis of Arterial Blood Gases A. pH 1. Normal: 7.35 – 3.45 2. Acidic: <7.35 3. Alkaline: >7.45 B. pCO2 Pressure of carbon dioxide; respiratory component 1. Normal: 35-45 mm Hg 2. Acidic: > 45 mm Hg (carbon dioxide forms carbonic acid) Hypercapnia: elevated levels of carbon dioxide in blood 3. Alkaline: < 35 mm Hg

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Hypocapnia: decreased levels of carbon dioxide in blood C. HCO3 Bicarbonate; renal or metabolic component 1. Normal: 22 – 26 mEq/L 2. Acidic: < 22 mEq/L 3. Alkaline: > 26 mEq/L D. Base Excess 1. Calculated value for buffer base capacity: the amount of acid or base added to blood to obtain a pH of 7.4 2. Normal: -3 -- +3 E. pO2 Pressure of oxygen in blood 1. Gives data about level of oxygenation; not used to calculate acid-base status of blood 2. Normal: 80 – 100 mm Hg 3. Hypoxemia: < 80 mm Hg IV. Acid-Base Imbalance A. Classifications 1. Acidosis or alkalosis a. Acidosis: Hydrogen ion concentration in blood increases above normal and pH is below 7.35 b. Alkalosis: Hydrogen ion concentration in blood decreases below normal and pH is above 7.45 2. Origin of the problem a. From the respiratory system b. From the metabolic system B. Disorders: Simple or Combined 1. Primary disorders a. Simple b. One cause, either respiratory or metabolic

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2. Combined disorders a. More severe b. Both the respiratory and metabolic systems are the cause of the same imbalance C. Compensation 1. Only occurs with primary disorders 2. Response by the system not causing the imbalance to correct the pH Example: with respiratory acidosis, the kidneys would eliminate hydrogen ions in urine to offset the acidosis caused by hypoventilation of lungs. 3. Complete Compensation occurs if the pH is corrected to the normal range (7.35 – 7.45) 4. Partial Compensation occurs if there is improvement in the pH but not to the normal range. 5. Compensation can be determined by analysis of the arterial blood gas results. D. Treatment 1. Urgency a. Mental ability and level of consciousness is often affected b. Brain function usually affected; brain cells need proper conditions to perform cellular functions c. Cells cannot function properly if significant acidosis or alkalosis occurs 2. Indirect treatment a. Treating and correcting the precipitating condition often corrects the acid-base imbalance b. Directly treating the acid-base imbalance, by adding or removing hydrogen or bicarbonate ions, may lead to further imbalances c. Not usually first line of treatment

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V. Types of Acid-Base Imbalances A. Respiratory Acidosis pH < 7.35 pCO2 > 45 mm Hg (excess carbon dioxide in the blood) Respiratory system impaired and retaining CO2; causing acidosis 1. Common Stimuli a. Acute respiratory failure from airway obstruction b. Over-sedation from anesthesia or narcotics c. Some neuromuscular diseases that affect ability to use chest muscles d. Chronic respiratory problems, such as Chronic Obstructive Lung Disease 2. Signs and Symptoms a. Compensation: kidneys respond by generating and reabsorbing bicarbonate ions, so HCO3 >26 mm Hg b. Respiratory: hypoventilation, slow or shallow respirations c. Neuro: headache, blurred vision, irritability, confusion d. Respiratory collapse leads to unconsciousness and cardiovascular collapse 3. Collaborative Care a. Early recognition of respiratory status and treat cause b. Restore ventilation and gas exchange; CPR for respiratory failure with oxygen supplementation; intubation and ventilator support if indicated c. Treatment of respiratory infections with bronchodilators, antibiotic therapy d. Reverse excess anesthetics and narcotics with medications such as naloxone (Narcan)

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e. Chronic respiratory conditions a. Breathe in response to low oxygen levels b. Adjusted to high carbon dioxide level through metabolic compensation (therefore, high CO2 not a breathing trigger) c. Cannot receive high levels of oxygen, or will have no trigger to breathe; will develop carbon dioxide narcosis d. Treat with no higher than 2 liters O2 per cannula f. Continue respiratory assessments, monitor further arterial blood gas results 4. Nursing Diagnoses a. Impaired Gas Exchange b. Ineffective Airway Clearance B. Respiratory Alkalosis pH < 7.35 pCO2 < 35 mm Hg. Carbon dioxide deficit, secondary to hyperventilation 1. Common Stimuli a. Hyperventilation with anxiety from uncontrolled fear, pain, stress (e.g. women in labor, trauma victims) b. High fever c. Mechanical ventilation, during anesthesia 2. Signs and Symptoms a. Compensation: kidneys compensate by eliminating bicarbonate ions; decrease in bicarbonate HCO3 < 22 mm Hg. b. Respiratory: hyperventilating: shallow, rapid breathing

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c. Neuro: panicked, light-headed, tremors, may develop tetany, numb hands and feet (related to symptoms of hypocalcemia; with elevated pH more Ca ions are bound to serum albumin and less ionized “active” calcium available for nerve and muscle conduction) d. May progress to seizures, loss of consciousness (when normal breathing pattern returns) e. Cardiac: palpitations, sensation of chest tightness 3. Collaborative Care a. Treatment: encourage client to breathe slowly in a paper bag to rebreathe CO2 b. Breathe with the patient; provide emotional support and reassurance, anti-anxiety agents, sedation c. On ventilator, adjustment of ventilation settings (decrease rate and tidal volume) d. Prevention: pre-procedure teaching, preventative emotional support, monitor blood gases as indicated C. Metabolic Acidosis pH <7.35 Deficit of bicarbonate in the blood NaHCO3 <22 mEq/L Caused by an excess of acid, or loss of bicarbonate from the body 1. Common Stimuli a. Acute lactic acidosis from tissue hypoxia (lactic acid produced from anaerobic metabolism with shock, cardiac arrest) b. Ketoacidosis (fatty acids are released and converted to ketones when fat is used to supply glucose needs as in uncontrolled Type 1 diabetes or starvation)

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c. Acute or chronic renal failure (kidneys unable to regulate electrolytes) d. Excessive bicarbonate loss (severe diarrhea, intestinal suction, bowel fistulas) e. Usually results from some other disease and is often accompanied by electrolyte and fluid imbalances f. Hyperkalemia often occurs as the hydrogen ions enter cells to lower the pH displacing the intracellular potassium; hypercalcemia and hypomagnesemia may occur 2. Signs and Symptoms a. Compensation: respiratory system begins to compensate by increasing the depth and rate of respiration in an effort to lower the CO2 in the blood; this causes a decreased level of carbon dioxide: pCO2 <35 mm HG. b. Neuro changes: headache, weakness, fatigue progressing to confusion, stupor, and coma c. Cardiac: dysrhythmias and possibly cardiac arrest from hyperkalemia d. GI: anorexia, nausea, vomiting e. Skin: warm and flushed f. Respiratory: tries to compensate by hyperventilation: deep and rapid respirations known as Kussmaul’s respirations g. Diagnostic test findings: 1. ABG: pH < 7.35, HCO3 < 22 2. Electrolytes: Serum K+ >5.0 mEq/L 3. Serum Ca+2 > 10.0 mg/dL 4. Serum Mg+2 < 1.6 mg/dL 3. Collaborative Care a. Medications: Correcting underlying cause will often improve acidosis

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b. Restore fluid balance, prevent dehydration with IV fluids c. Correct electrolyte imbalances d. Administer Sodium Bicarbonate IV, if acidosis is severe and does not respond rapidly enough to treatment of primary cause. (Oral bicarbonate is sometimes given to clients with chronic metabolic acidosis) Be careful not to overtreat and put client into alkalosis e. As acidosis improves, hydrogen ions shift out of cells and potassium moves intracellularly. Hyperkalemia may become hypokalemia and potassium replacement will be needed. f. Assessment 1. Vital signs 2. Intake and output 3. Neuro, GI, and respiratory status; 4. Cardiac monitoring 5. Reassess repeated arterial blood gases and electrolytes 4. Nursing Diagnoses a. Decreased Cardiac Output b. Risk for Excess Fluid Volume c. Risk for Injury D. Metabolic Alkalosis pH >7.45 HCO3 > 26 mEq/L Caused by a bicarbonate excess, due to loss of acid, or a bicarbonate excess in the body 1. Common Stimuli a. Loss of hydrogen and chloride ions through excessive vomiting, gastric suctioning, or excessive diuretic therapy b. Response to hypokalemia

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c. Excess ingestion of bicarbonate rich antacids or excessive treatment of acidosis with Sodium Bicarbonate 2. Signs and Symptoms a. Compensation: Lungs respond by decreasing the depth and rate of respiration in effort to retain carbon dioxide and lower pH b. Neuro: altered mental status, numbness and tingling around mouth, fingers, toes, dizziness, muscle spasms (similar to hypocalcemia due to less ionized calcium levels) c. Respiratory: shallow, slow breathing d. Diagnostic test findings 1. ABG’s: pH> 7.45, HCO3 >26 2. Electrolytes: Serum K+ < 3.5 mEq/L 3. Electrocardiogram: as with hypokalemia 3. Collaborative Care a. Correcting underlying cause will often improve alkalosis b. Restore fluid volume and correct electrolyte imbalances (usually IV NaCl with KCL). c. With severe cases, acidifying solution may be administered. d. Assessment 1. Vital signs 2. Neuro, cardiac, respiratory assessment 3. Repeat arterial blood gases and electrolytes 4. Nursing Diagnoses a. Impaired Gas Exchange b. Ineffective Airway Clearance c. Risk for Injury

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