Here are the key characteristics of minor burns: - Partial thickness burns cover no more than 15% of total body surface area (TBSA) - Full thickness burns cover less than 2% of TBSA - Burn areas do not involve sensitive areas like eyes, ears, hands, face, feet or perineum - There are no electrical burns or evidence of inhalation injury

1. Fluids andElectrolytes Ma. Tosca Cybil A. Torres, RN, MAN

2. OBJECTIVES After this lecture/discussion, the learner should be able to: 1. Describe the mechanisms that maintain fluid, electrolyte and acid-base balance. 2. Compare the mechanisms and effects of fluid deficit and excess. 3. Discuss the mechanisms and effects of deficits and excess. 4. Describe the mechanisms that maintain acid-base balance. 5. Differentiate between metabolic and respiratory acidosis and alkalosis. 6. Apply the pathophysiologic principles of acid-base balance to the interpretation of ABG measurements. 7. Analyze the components of ABGs to identify the type of acid-base balance. 8. Describe the causes and effects of each type of acid-base balance. 9. Use ABG findings in formulating the care of the patient with an acid-base imbalance. 10. Describe the management of patients with a fluid, electrolyte, or acid-base imbalance.

3. Fluids

5. Water provides a medium for transporting nutrients to cells and wastes from cells and for transporting substances such as hormones, enzymes, blood platelets, and red and white blood cells

6. Water facilitates cellular metabolism and proper cellular chemical functioning

7. Water acts as a solvent for electrolytes and nonelectrolytes

8. Helps maintain normal body temperature

9. Facilitates digestion and promotes elimination

11. VARIATIONS IN FLUID CONTENT 50% Adult Female 60% Adult Male 45% Elderly 77% Infants AGE

14. AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODY

15. ANTIDIURETIC HORMONE REGULATION MECHANISMS Osmoreceptors in hypothalamus ↑Osmolarity Hypothalamus ↓ Posterior pituitary gland ↓Blood volume or ↓BP Volume receptor Atria and great veins Kidney tubules ↑ADH ↑H2O reabsorption Narcotics, Stress, Anesthetic agents, Heat, Nicotine, Antineoplastic agents, Surgery ↑vascular volume and ↓osmolarity

16. ALDOSTERONE-RENIN-ANGIOTENSIN SYSTEM RENIN Juxtaglomerular cells-kidney Angiotensinogen in plasma ↓Serum Sodium ↓Blood volume Angiotensin I Angiotensin-converting enzyme Via vasoconstriction of arterial smooth muscle ↑Sodium resorption (H2O resorbed with sodium); ↑ Blood volume Angiotensin II Kidney tubules ALDOSTERONE Adrenal Cortex Intestine, sweat glands, Salivary glands

17. Fluid Types Fluids in the body generally aren’t found in pure forms Isotonic, hypotonic, and hypertonic types Defined in terms of the amount of solute or dissolve substances in the solution Balancing these fluids involves the shifting of fluid not the solute involved

18. Isotonic Solutions No net fluid shifts occur between isotonic solutions because the solution are equally concentrated Ex. NSS or 0.9SS

19. Hypotonic Solutions Has a lower solute concentration than another solution Fluid from the hypotonic solution would shift into the second solution until the two solutions had equal concentrations Ex. Half normal or 0.45%SS

20. Hypertonic Solutions Has a higher solute concentration than another solution Fluid from the second solution would shift into the hypertonic solution until the two solutions had equal concentrations Ex. D5NSS

21. Fluid Movements Fluids and solutes constantly move within the body, which allows the body to maintain homeostasis Fluids along with nutrients and waste products constantly shift within the body’s compartments from the cell to the interstitial spaces, to the blood vessels and back again

22. Fluid Movements Types of Transport A. Active transport B. Passive transport Diffusion Osmosis Filtration

23. Assessment CLINICAL MEASUREMENT Daily weights Each kg = 1 L of fluid To gain accuracy: Balance the scale before each use and weigh the client; At same time each day before breakfast after the first void Wear the same or similar clothing On the same scale Vital signs Tachycardia – first sign of hypovolemia Fluid I & O Oral fluids Ice chips Foods that tend to become fluid at room temperature Tube feedings Parenteral fluids IV meds Catheter or tube irrigant Urinary output – if with diaper, 1 g = 1 mL Vomitus or liquid feces Diaphoresis Tube drainage Wound dressing or wound fistula

24. LABORATORY TESTS FOR EVALUATING FLUID STATUS Osmolality – measures the solute concentration per kilogram in blood and urine. Osmolarity – concentration of solution per liter. BUN – (10-20 mg/dL)made up of urea, an end product of protein metabolism by the liver. Creatinine (0.7 to 1.5 mg/dL)- end product of muscle metabolism Serum electrolytes CBC

25. Diagnosis Fluid volume deficit High risk for Fluid volume deficit Fluid volume excess Altered oral mucous membrane

27. Change in sodium/water ratio = either hypoosmolarity or hyperosmolarity

28. Fluid excess or deficit = loss of fluid balance

29. As with all clinical problems, the same pathophysiologic change is not of equal significance to all people

30. For example, consider two persons who have the same viral syndrome with associated nausea and vomitingMan with renal failure Life threatening E+ disturbances ECF Volume Depletion No Significant E+ disturbances

31. FLUID DEFICIT/HYPOVOLEMIA May occur as a result of: Reduced fluid intake Loss of body fluids Sequestration (compartmentalizing) of body fluids Pathophysiology and Clinical Manifestations DECREASED FLUID VOLUME Stimulation of thirst center in hypothalamus ↑ ADH Secretion Renin-Angiotensin-Aldosterone System Activation ↑ Water resorption Person complains of thirst ↑ Sodium and Water Resorption ↓ Urine Output ↑ Urine specific gravity

32. Pathophysiology and Clinical Manifestations UNTREATED FLUID VOLUME DEFICIT Depletion of fluids available ↑ BODY TEMPERATURE Cells become unable to continue providing water to replace ECF losses Dry mucous membranes Signs of circulatory collapse ↓ blood pressure ↑ heart rate ↑ respiratory rate Difficulty with speech Restlessness and Apprehension

33. Hypovolemia Nursing Intervention Monitor fluid intake and output Checked daily weight (a 1lb(0.45kg) weight loss equals a 500 ml fluid loss) Monitor hemodynamic values such as CVP Monitor results of laboratory studies Assess level of consciousness Administer and monitor I.V. fluids Apply and adjust oxygen therapy as ordered If patient is bleeding, apply direct continuous pressure to the area and elevate it if possible Assess skin turgor Assess oral mucous membranes Turn the patient at least every 2 hours to prevent skin breakdown Encourage oral fluids

34. Hypovolemia Warning Signs Cool pale skin over the arms and legs Decreased central venous pressure Delayed capillary refill Deterioration in mental status flat jugular veins Orthostatic hypotension Tachycardia Urine output initially more than 30ml/min, then dropping below 10ml/hour Weak or absent peripheral pulses Weight loss

35. Collaborative Care Management Identification of vulnerable patients and risk factors: * Compromised mental state * Physical limitations * Disease states * Limited access to adequate food and fluids Development of a plan of care Family members should be educated about the importance of fluid and nutrition intake Collaboration with the nurse, patient, family members, and other health care providers for continued assessment and treatment of problems Ongoing assessment and detailed action plan of fluid and serum electrolyte balance. Factors such as medications (particularly diuretics), hyperventilation, fever, burns, diarrhea, and diabetes with appropriate referral

36. Collaborative Care Key Points 1 Liter of water = 1 kg of water by weight Fluid replacement are calculated according to this ratio plus 1.5 L to fulfill the current daily needs For example, JUAN, a one-year-old, lost 1 kg of water from diarrhea as weighed from his diaper over the last 24 hours. Therefore, since 1 kg=1 L, fluid replacement therapy for him will involve 1 L of fluids + 1500 L. Oral fluid resuscitation is preferable but if the patient is unable to tolerate fluids, IV Therapy may be ordered Vital signs should be assessed regularly Postural hypotension is common for postural persons with fluid volume deficit. How do we assess this? For example, in the care of LOIDA, a 31 year old with severe DHN, you take her blood pressure (130/80) and pulse (75) while she’s lying down. Then you ask her to sit at the edge of bed. When you take her blood pressure again, you get 115/80 and when you take her pulse, you get 80. This is consistent with intravascular volume depletion. Daily weighing is also useful to monitor fluid and electrolyte balance Laboratory results should be reviewed for various fluid and electrolyte disturbances so that appropriate adjustments to therapy can be initiated

37. Fluid Replacement Therapy Aimed at restoring and maintaining homeostasis Methods: Oral and gastric feeding Parenteral therapy Choice of therapy affected by several factors Type and severity of imbalance Patient’s overall health status, age, renal and cardiovascular status Usual maintenance requirements

38. Fluid Replacement Therapy Advantages Provides the patient with life-sustaining fluids, electrolytes, and drugs Immediate and predictable therapeutic effects Preferred for administering fluids, electrolytes, and drugs in emergency situations Allows fluid intake when a patient has GI malabsorption Permits accurate dosage titration for analgesics and other drugs

39. Fluid Replacement Therapy Disadvantages Solution incompatibility Adverse reactions Infection

40. Fluid Replacement Therapy Administration routes Oral route : oral ingestion of fluids and electrolytes as liquids or solids administered directly into the GI tract Nasogastric route: instillation of fluids and electrolytes through feeding tubes, such as NG, gastrostomy and jejunostomy tubes I.V. route: administration of fluids and electrolytes directly into the bloodstream using continuous infusion, bolus, or I.V. push injection through peripheral or central venous site

41. Which among the following IV solutions contains the highest potassium content?A. D5 IMBB. Lactated Ringer's SolutionC. D5 LRSD. D5 0.3 NaCl

42. Composition of Different Intravenous Solution

43. Fluid Replacement TherapyISOTONIC SOLUTION

44. Fluid Replacement TherapyHYPOTONIC SOLUTION

45. Fluid Replacement TherapyHYPERTONIC SOLUTION

46. FLUID EXCESS/HYPERVOLEMIA Renal and endocrine disturbances, malignancies, adenomas Psychiatric Disorders, SIADH, Certain head injuries Dietary Sodium Indiscretion Failure of renal or hormonal regulatory functions Excessive Sodium Intake Overhydration FLUID VOLUME EXCESS/HYPERVOLEMIA Sodium ADH Extracellular volume expands Fluid becomes progressively hyponatremic Normal Extracellular fluid Normal sodium concentration Renal Tubules

48. Thus there, is an increase in intracellular fluid

49. The brain cells are particularly sensitive to the increase of intracellular water, the most common signs of hypoosmolaroverhydration are changes in mental status. Confusion, ataxia, and convulsions may also occur.

51. Hypervolemia Diagnostic Findings: Decreased hematocrit resulting from hemodilution Normal serum Na level Low serum K and BUN levels either due to hemodilution or higher levels may indicate renal failure Low oxygen level Abnormal chest x-ray Indicates fluid accumulation May reveal pulmonary edema or pleural effusions

52. Hypervolemia Treatment Na and fluid intake restriction Diuretics to promote excess fluid excretion Morphine and nitroglycerin (Nitro-Dur) for pulmonary edema Dilate blood vessels Reduce pulmonary congestion and amount of blood returning to the heart Digoxin for heart failure Strengthens cardiac contractions

53. Hypervolemia Treatment Supportive measures Oxygen administration Bed rest Hemodialysis or continuous renal replacement therapy for renal dysfunction

54. Hypervolemia Nursing Interventions Monitor fluid intake and output Monitor daily weight Monitor cardiopulmonary status Auscultate breathe sounds Assess for complaints of dyspnea Monitor chest x-ray results Monitor arterial blood gas values Assess for peripheral edema Inspect the patient for sacral edema Monitor infusion of I.V. solutions Monitor the effects of prescribed medications

55. BURN

56. General Information Involve destruction of the epidermis, dermis, or subcutaneous layers of the skin Can be permanently disfiguring and incapacitating and possibly life-threatening

57. General Information Associated imbalances result from alterations in skin integrity and internal body membranes, and from effect of heat on body water and solute loss that may result from cellular destruction

58. General Information Type and severity of imbalance depends on burn type and depth, percentage body surface area involved and burn phase

59. Pathophysiology Burn phase Fluid- accumulation phase Fluid-remobilization phase Convalescent phase Burn Phase: Refer to stages that describe physiologic changes occurring after a burn

61. Last fro 36 to 48 hours after a burn injury

62. Fluid shifts from vascular compartment to interstitial space – third-space shift

63. Edema caused by shifted fluid, which typically reaches maximum within 8 hours after injury

66. Muscle and tissue injuries

67. GI problems

68. Electrolyte imbalances:

70. Also known as diuresis stage

71. Starts about 48 hours after initial burn

72. Fluid shifted back to vascular compartment

73. Edema at burn site decreased, blood flow to kidneys increased, increased urine output

75. Begins after first two phases has been resolved

76. Characterized by healing or reconstruction of burn wound

77. Major fluid shifts now resolved but possible further fluid and electrolyte imbalances exist as a result of inadequate dietary intake

79. Characteristics 2. Moderate Burns Partial thickness burns are deep and are 15% to 25% of the TBSA in the adult Full thickness burns are 2% to 10% of the TBSA in the adult Burn areas do not involve the eyes, ears, hands, face, feet, or perineum There are no electrical burns or inhalation injuries The client is an adult younger than 60 y.o. The client has no chronic cardiac, pulmonary, or endocrine disorder at the time of the burn injury No other complicated injury occurred with the burn

80. Characteristics 3. Major Burns Partial thickness burns are > 25% of the TBSA in the adult Full thickness burns are > 10% of the TBSA Burn areas involve the eyes, ears, hands, face, feet, or perineum The burn injury was an electrical or inhalation injury The client is older than 60 y.o. The client has a chronic cardiac, pulmonary, or metabolic disorder at the time of the burn injury Burns are accompanied by other injuries

81. Reparative Process Assessment of Extent Extent / Degree In about 5 days, epidermis peels, heals spontaneously. Itching and pink skin persist for about a week. No scarring. Heals spont. If it does not become infected w/in 10 days - 2 weeks. Pink to red: slight edema, which subsides quickly. Pain may last up to 48 hours. Relieved by cooling. Sunburn is a typical example. First Degree Takes several weeks to heal. Scarring may occur. Takes several weeks to heal. Scarring may occur. Superficial: Pink or red; blisters form (vesicles); weeping, edematous, elastic. Superficial layers of skin are destroyed; wound moist and painful. Deep dermal: Mottled white and red: edematous reddened areas blanch on pressure. May be yellowish but soft and elastic – may or may not be sensitive to touch; sensitive to cold air. Hair does not pull out easily Second degree Assessment of Burn Injury

82. Reparative Process Assessment of Extent Extent / Degree Eschar must be removed. Granulation tissue forms to nearest epithelium from wound margins or support graft. For areas larger than 3-5 cm, grafting is required. Expect scarring and loss of skin function. Area requires debridement, formation of granulation tissue, and grafting. Destruction of epithelial cells – epidermis and dermis destroyed Reddened areas do not blanch with pressure. Not painful; inelastic; coloration varies from waxy white to brown; leathery devitalized tissue is called eschar. Destruction of epithelium, fat, muscles, and bone. Third degree Assessment of Burn Injury

83. Burn:Classification Superficial (1° burns) Involve only the epidermal layer of the skin. sunburns are commonly first-degree burns. 59

84. 1° burn 2° burn 60

85. 61 Superficial burn (1° burn)

86. 62 Present of blisters indicates superficial partial-thickness injury. Blister may ↑size because continuous exudation and collection of tissue fluid. Healing phase of partial thickness, itching and dryness because ↑vascularization of sebaceous glands, ↓reduction of secretions and ↑perspiration. Partial thickness (2°burn)

87. 2° burn 63

88. 64 Partial thickness (2°burn)

89. Burn:Classification 3.Full thickness (third-degree burn) Destruction of the epidermis and the entire dermis, subcutaneous layer, muscle and bone. Nerve ending are destroyed-painless wound. Eschar may be formed due to surface dehydration. Black networks of coagulate capillaries may be seen. Need skin grafting because the destroyed tissue is unable to epithelialize. Deep partial-thickness burn may convert to a full-thickness burn because of infection, trauma or ↓blood supply. 65

90. 3° burn 66

91. Eschar:composed of denatured protein 67

92. 68 Full thickness (3°burn)

93. Extent of surface area burned Rule ofnines-An estimated of the TBSA involved as a result of a burn. The rule of nines measures the percentage of the body burned by dividing the body into multiples of nine. The initial evaluation is made upon arrival at the hospital. 69

94. Lund and Browder More precise method of estimating Recognizes that the percentage of BSA of various anatomic parts. By dividing the body into very small areas and providing an estimate of proportion of BSA accounted for by such body parts Includes, a table indicating the adjustment for different ages Head and trunk represent larger proportions of body surface in children. 70

95. 71

96. Lund and Browder chart 72

97. TYPES OF BURNS Thermal Burns: caused by exposure to flames, hot liquids, steam or hot objects Chemical Burns: Caused by tissue contact with strong alkali, or organic compounds Systemic toxicity from cutaneous absorption can occur Radiation Burns: caused by exposure to UV light, x-rays, or radioactive source

98. TYPES OF BURNS Electrical Burns: Caused by heat generated by electrical energy as it passes through the body Results in internal tissue damage Cutaneous burns cause muscle and soft tissue damage that may be extensive, particularly in high voltage electrical injuries Alternating current is more dangerous than direct current because it is associated with CP arrest, ventricular fibrillation, tetanic muscle contractions, and long bone or vertebral fractures

100. Approximately 10% of plasma volume lost into tissue soon after a severe burn

101. Occurs because of the third space shift causes multiple effects:

102. With burn’s damage to the skin surface, decrease in skins ability to prevent water loss; patient can lose up to 8L of fluid per day (400ml/hour)

104. Potential Imbalance Hyperkalemia / Hypokalemia Hypocalcemia Hyponatremia / Hypernatremia Metabolic acidosis Respiratory acidosis

105. Burns NURSING PRIORITY: The client with burn injury is often awake, mentally alert, and cooperative at first. The level of consciousness may change as respiratory status change or as the fluid shift occurs, precipitating hypovolemia. If the client is unconscious or confused, assess him or her for the possibility of a head injury.

106. Burns Assess for Patent airway Presence of adequate breath sounds Symptoms of hypoxia Pulmonary damage Burns around the face, neck, mouth or in the oral mucosal area Circulatory status Tachycardia and hypotension occur early Elevate UO

107. Burns Assess for GI function – check last time client ate Fluid status UO (30 ml/hr) Hypotension (< 90/60) Confusion / disorientation Circulatory status of the extremities

109. Respiratory status takes priority over the treatment of the burn injury

110. If burn area is small  cold compress or immerse in cool water (not ice) to ↓ heat

111. May have ointment on the burn area

113. Burns First 24 hours

114. Burns Second 24 hours

116. Mortality rates are higher for children < 4 y.o, particularly those < 1 y.o., and for clients over the age of 60 years.

117. Debilitating disorders, such as cardiac, respiratory, endocrine, and renal d/o, negatively influence the client’s response to injury and treatment.

119. Which one is not a cation?A. Calcium B. Magnesium C. Phosphorous D. Sodium

120. Anions and Cations Anions Cations Calcium Magnesium Potassium Sodium Bicarbonate Chloride Phosphorous

122. WHAT DO ELECTROLYTES DO? Promote neuromuscular irritability Maintain body fluid volume and osmolarity Distribute body water between fluid compartments Regulate acid-base balance

124. Its concentration is the major determinant of ECF volume

125. Is the chief electrolyte of ECF

126. Influence ICF Volume

127. Participates in the generation and transmission of nerve impulses

128. Is an essential electrolyte in the sodium-potassium pump

129. RDA: not known precisely. 500 mg

130. Eliminated primarily by the kidneys, smaller in feces and perspiration

131. Salt intake affects sodium concentrations

132. Sodium is conserved through reabsorption in the kidneys, a process stimulated by aldosterone

134. PATHOPHYSIOLOGY OF HYPONATREMIA Sodium loss from the intravascular compartment Diffusion of water into the interstitial spaces Sodium in the interstitial space is diluted Decreased osmolarity of ECF Water moves into the cell as a result of sodium loss Extracellular compartment is depleted of water CLINICAL SYMPTOMS

135. CLINICAL MANIFESTATIONS OF HYPONATREMIA Muscle Weakness APATHY Postural hypotension Nausea and Abdominal Cramps Weight Loss In severe hyponatremia: mental confusion, delirium, shock and coma

136. COLLABORATIVE CARE MANAGEMENT General goal: correct sodium imbalance and restore normal fluid and electrolyte homeostasis Recognition of people at risk for hyponatremia is essential for its prevention: athletes, persons working in hot environments Salt is always replaced along with water Management includes educating vulnerable people to recognize signs and symptoms of sodium depletion and maintaining sufficient sodium and water intake to replace skin and insensible fluid loss Generally, an increased sodium and water intake provides adequate treatment Education as the importance of sodium and fluid balance and the rationale for prescription medications to ensure compliance Daily weight. MIO Monitoring of sodium levels to determine extent of replacement Generally, PNSS or PLRS is prescribed Too rapid restoration of sodium balance, hypertonic sodium solutions may provoke brain injury

137. HYPERNATREMIA A serum sodium level above 145 mEq/L is termed hypernatremia May occur as a result of fluid deficit or sodium excess Frequently occurs with fluid imbalance Develops when an excess of sodium occurs without a proportional increase in body fluid or when water loss occurs without proportional loss of sodium Risk Factors: excess dietary or parenteral sodium intake, watery diarrhea, diabetes insipidus, damage to thirst center, those with physical or mental status compromise, and people with hypothalamic dysfunction

138. PATHOPHYSIOLOGY OF HYPERNATREMIA Increased Sodium concentration in ECF Osmolarity rises Water leaves the cell by osmosis and enters the the extracellular compartments Dilution of fluids in ECF Cells are water depleted CLINICAL SYMPTOMS Suppression of aldosterone secretion Sodium is exreted in the urine

139. CLINICAL MANIFESTATIONS Dry, sticky mucous membranes Firm, rubbery tissue turgor DEATH Tachycardia Manic excitement

140. COLLABORATIVE CARE MANAGEMENT Recognition of risk factors: bedridden and debilitated patients, diabetes insipidus, fluid deprivation, the elderly and the very young A careful and accurate record of MIO permits quick recognition of negative fluid balance People with kidney failure, CHF, or increased aldosterone production may require dietary sodium intake restriction Usually, osmolar balance can be restored with oral fluids. If not, the parenteral route may be necessary Fluid resuscitation must be undertaken with particular caution in patients with compromised cardiac or renal function The nurse should closely monitor the patient’s response to fluids and be alert to symptoms of fluid overload

142. The more K, the less Na. The less K, the more Na

143. Plays a vital role in such processes such as transmission of electrical impulses, particularly in nerve, heart, skeletal, intestinal and lung tissue; CHON and CHO metabolism; and cellular building; and maintenance of cellular metabolism and excitation

144. Assists in regulation of acid-base balance by cellular exchange with H

145. RDA: not known precisely. 50-100 mEq

146. Sources: bananas, peaches, kiwi, figs, dates, apricots, oranges, prunes, melons, raisins, broccoli, and potatoes, meat, dairy products

147. Excreted primarily by the kidneys. No effective conserving mechanism

148. Conserved by sodium pump and kidneys when levels are low

149. Aldosterone triggers K excretion in urine

151. PATHOPHYSIOLOGY OF HYPOKALEMIA = Action Potential Nerve and Muscle Activity The cell becomes less excitable Low Extracellular K+ Increase in resting membrane potential

152. Aldosterone is secreted Sodium is retained in the body through resorption by the kidney tubules Potassium is excreted Use of certain diuretics such as thiazides and furosemide, and corticosteroids Increased urinary output Loss of potassium in urine

153. COLLABORATIVE CARE MANAGEMENT Being alert to the conditions that cause potassium depletion such as vomiting, diarrhea and diuretics, by monitoring the patient for early warning signs No more than 3 enemas without consulting a physician Education about the importance of adequate dietary intake of potassium In severe hypokalemia, a patient may die unless potassium is administered promptly The safest way to administer K is orally. When K is given IV, the rate of flow must be monitored closely and should be diluted. Should not exceed 20 mEq/hr If PO, taken with at least ½ glass of water Cardiac monitoring is useful Potassium sparing diuretics such as triamterene, spironolactone, etc Symptoms of K depletion: muscle weakness, anorexia, nausea and vomiting = appropriate referral

156. Potassium-wasting diuretics may be prescribed to promote further potassium loss. Dialysis for patients with renal failure to eliminate excess potassium

157. Intravenous Ca Gluconate may be prescribed to counteract the cardiac effects of hyperkalemia

159. Close link between calcium and phosphorus. High PO4, Low Ca

160. Necessary for nerve impulse transmission and blood clotting and is also a catalyst for muscle contraction and other cellular activities

161. Needed for Vitamin B12 absorption and use

162. Necessary for strong bones and teeth and thickness and strength of cell membranes

163. RDA: 1g for adults. Higher for children and pregnant and lactating women according to body weight, older people, esp. post-menopausal

164. Found in milk, cheese, and dried beans; some in meat and vegetables

165. Use is stimulated by Vitamin D. Excreted in urine, feces, bile, digestive secretions, and perspiration

168. Calcium and Sodium repel each other

169. When serum calcium levels are low, this blocking effect is minimized

170. When Sodium moves more easily into the cell, depolarization takes place more easily

171. This results in increased excitability of the nervous system leading to muscle spasm, tingling sensations, and if severe, convulsions and tetany

172. Skeletal, smooth, and cardiac muscle functions are all affected by overstimulationCELL Calcium Sodium

173. CLINICAL MANIFESTATIONS OF HYPOCALCEMIA PAINFUL MUSCULAR SPASMS (TETANY) ESPECIALLY OF FEET AND HANDS (CARPOPEDAL SPASMS), MUSCLE TWITCHING AND CONVULSIONS MAY FOLLOW TREATMENT COMPLAINT OF NUMBNESS AND TINGLING OF EARS, NOSE, FINGERTIPS OR TOES

174. TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY TROUSSEAU'S SIGN CHVOSTEK'S SIGN

175. COLLABORATIVE CARE MANAGEMENT Identify risk factors: Inadequate calcium intake, excess calcium loss, Vitamin D deficiency, patients with poor diets Education about the importance of adequate calcium and Vitamin D intake Patients undergoing thyroid, parathyroid, and radical neck surgery are particularly vulnerable to hypocalcemia secondary to parathyroid hormone deficit Monitoring of serum calcium levels and correction of deficits Citrate is added to store blood to prevent coagulation. Citrate + Transfusion = Citrate+Calcium Normally, Liver + Citrate = Quick metabolism Preexisting calcium deficit/hepatic dysfunction/large amounts of BT very rapidly = hypocalcemia With acute hypocalcemia, Ca Gluconate is used + Continuous cardiac monitoring Mild Hypocalcemia: High calcium diet or oral calcium salts If PTH or Vit D Deficiency is the cause: aluminum hydroxide gel is used because when serum phosphate level rises, calcium level falls Complication: Bone demineralization Therefore, careful ambulation should be encouraged to minimize bone resorption

176. HYPERCALCEMIA: Serum concentration > 10mg/dLCauses and Effects Loss from bones Immobilization, Carcinoma with bone metastases, Multiple myeloma Excess Intake ↑ Calcium diet (esp. milk) Antacids containing calcium Increase in factors Causing Mobilization from bone ↑PTH, ↑ Vitamin D, steroid therapy HYPERCALCEMIA CNS ↓Deep-tendon reflexes ↓ Lethargy ↓ Coma Muscles Muscle fatigue, hypotonia ↓ ↓ GI motility Kidneys Stones ↓ Kidney Damage Bones Bone pain ↓ Osteoporosis ↓ Fractures CV System Depressed activity ↓ Dysrhythmias ↓ Cardiac Arrest

177. HOW IT HAPPENS HYPERCALCEMIA DEPRESSED NERVE AND MUSCLE ACTIVITY DEEP TENDON REFLEXES MAY BE DECREASED OR ABSENT MYOCARDIAL FUNCTION IS ALTERED

178. CLINICAL MANIFESTATIONS OF HYPERCALCEMIA Constipation Cardiac Dysrhythmias Nausea Decreased GI Motility Mental status changes: lethargy, confusion, memory loss

179. CLINICAL MANIFESTATIONS OF HYPERCALCEMIA Calcium accumulates in the ECF and passes through the kidneys Immobilization Bone Demineralization Calcium Stones Ca Precipitation

180. COLLABORATIVE CARE MANAGEMENT Mild hypercalcemia: hydration and education about avoiding foods high in calcium or medications that promote calcium elevation Ambulation as appropriate; weight-bearing exercises as tolerated Trapeze, resistance devices Marked hypercalcemia: prevention of pathologic fractures, individualized plan of care Prevention of renal calculi: encourage oral fluids to prevent concentrated urine: 3000 to 4000 mL/day unless contraindicated Acid-ash fruit juices: cranberry juice and prune juice Severe hypercalcemia: medical emergency: continuous cardiac monitoring, hydration, IV furosemide, Calcitonin and/or plicamycin (mithramycin), q2 serum and urinary electrolytes

182. Second most important cation in the ICF, 2nd to K+

183. Functions: Metabolism of CHO and CHON, protein and DNA synthesis, DNA and RNA transcription, and translation of RNA, maintains normal intracellular levels of potassium, helps maintain electric activity in nervous tissue membranes and muscle membranes

184. RDA: about 18-30 mEq; children require larger amounts

185. Sources: vegetables, nuts, fish, whole grains, peas, and beans

186. Absorbed in the intestines and excreted by the kidneys

188. PATHOPHYSIOLOGY OF HYPOMAGNESEMIA Low serum magnesium level Increased acetylcholine release Increased neuromuscular irritability Increased sensitivity to acetylcholine at the myoneural junction Diminished threshold of excitation for the motor nerve Enhancement of myofibril contraction

189. PATHOPHYSIOLOGY OF HYPOMAGNESEMIA High Serum Calcium Increased acetylcholine release Increased neuromuscular irritability Increased sensitivity to acetylcholine at the myoneural junction Diminished threshold of excitation for the motor nerve Enhancement of myofibril contraction Excretion of Magnesium By the GI tract High Serum Calcium

190. PATHOPHYSIOLOGY OF HYPOMAGNESEMIA MAGNESIUM INHIBITS TRANSPORT OF PTH DECREASE IN THE AMOUNT OF CALCIUM BEING RELEASED FROM THE BONE POSSIBLE CALCIUM DEFICIT

191. CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA DEPRESSION CONFUSION CRAMPS TETANY CONVULSIONS

192. COLLABORATIVE CARE MANAGEMENT Recognition of people at risk: people taking loop diuretics and digoxin should be encouraged to eat foods rich in magnesium, such as fruits, vegetables, cereals, and milk Recognition of signs and symptoms of magnesium deficiency Magnesium is essential for potassium resorption, so if hypokalemia does not respond to potassium replacement, hypomagnesemia should be suspected Treatment of the underlying cause is the first consideration in hypomagnesemia Severe: parenteral magnesium replacement is indicated IV therapy: continuous cardiac monitoring Safety measures for patients with mental status changes

193. HYPERMAGNESEMIA: Serum Mg level 2.5 mEq/L Seldom develops in the presence of normal renal function May occur as a result of Mg replacement May occur when MgSO4 is administered to prevent seizures resulting from eclampsia Careful monitoring is imperative

194. PATHOPHYSIOLOGY Renal failure, Excessive IV infusion of magnesium, Decreased GI elimination and/or absorption, etc. Accummulation of Mg in the body Mg Level Rises Altered Electrical Conduction Slowed heart rate and AV Block Diminishing of reflexes, drowsiness, lethargy Severe Respiratory Depression Peripheral vasodilation RESPIRATORY ARREST may occur Hypotension, flushing, and increased skin warmth

195. COLLABORATIVE CARE MANAGEMENT Identification of patients at risk: those with impaired renal function to avoid OTC that contain magnesium such as Milk of Magnesia and some Mg-containing antacids Any patient receiving parenteral magnesium therapy should be assessed frequently for signs of hypermagnesemia Mild hypermagnesemia: withholding magnesium-containing medications may suffice Renal failure: dialysis Severe: may require treatment with calcium gluconate (10-20 mL of 10% Ca Gluconate administered over 10 minutes) If cardiorespiratory collapse is imminent, the patient may require temporary pacemaker and ventilator support

196. NURSING MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCES

197. Parameter_____Fluid Excess___ Fluid Loss/Electrolyte Imbalance____ Behavior Tires easily; Change in behavior, confusion, apathy Head, neck Facial edema, distended neck Headache, thirst, dry mucous membranes veins Upper GI Anorexia, nausea, vomiting Skin Warm, moist, taut, cool feeling Dry, decreased turgor where edematous Respiration Dyspnea, orthopnea, productive Changes in rate and depth of respiration cough, moist breath sounds Circulation Loss of sensation in edematous Pulse rate changes, dysrhythmia, posturalareas, pallor, bounding pulse, increased blood pressure hypotension Abdomen Increased girth, fluid wave Distention, abdominal cramps Elimination Constipation Diarrhea, constipation Extremities Dependent edema, “pitting” Muscle weakness, tingling, tetany , discomfort from weight of bedclothes A

198. Refractory Edema Pitting edema Dependent edema

199. A LABORATORY VALUES FLUID DEFICITFLUID EXCESS Hemoconcentration Hemodilution ↑ Hct, BUN, E+ levels↓ Hct, BUN, E+ levels ↑ Urine Specific Gravity ↓ Urine Specific Gravity

200. Determined from analysis of patient data Diagnostic TitlePossible Etiologic Factors 1 Deficient fluid volume Active fluid volume loss (hemorrhage, diarrhea, gastric intubation, wounds, diaphoresis), inadequate fluid intake, failure of regulatory mechanisms, sequestration of body fluids 2 Excess Fluid Volume Excess fluid intake, excess sodium intake, compromised regulatory processes D

201. P EXPECTED PATIENT OUTCOMES 1. Will maintain functional fluid volume as evidenced by adequate urinary output, stable weight, normal vital signs, normal urine specific gravity, moist mucus membranes, balanced intake and output, elastic skin turgor, prompt capillary refill, and absence of edema 2. Will verbalize understanding of treatment plan and causative factors that led to the imbalance

202. 1,2 Intake and Output Monitoring - Type and amount of fluid the patient has received and the route by which they were administered - Record of solid food intake. Gelatin or Popsicles are recorded as fluids - Ice chips are recorded by dividing the amount of chips by ½ (60 mL of chips = 30 mL water) - Accurate output record and described by color, content, and odor (Normally, gastric contents are watery and pale yellow-green; they usually have a sour odor) - With acid-base balance upset, gastric secretions may have a fruity odor because of ketone bodies - Bile: thicker than gastric juice, dark green to brown, acrid odor, bitter taste when vomiting - NGT irrigation added to intake - Stools: difficult to estimate amount; consistency, color, and number of stools provide a reasonable estimate - Peritoneal or pleural fluid drainage is recorded as output as with its amount, color, and clarity - Character and volume of urine. Place signs and materials so that an accurate record of UO is maintained I

203. 1,2 Intake and Output Monitoring - Evaluate and refer urine specific gravity as appropriate (normal value is 1.003 – 1.030). The implications are: High Dehydration Low SIADH, overhydration - Drainage, fluid aspirated from any body cavity must be measured. With dressings, fluid loss is the difference between the wet dressings and the dry weight of the dressing - Accurate recording of the temperature to help the physician determine how much fluid should be replaced 1,2 Daily Weight - Evaluate trends in weight (An increase in 1kg in weight is equal to the retention of 1L of fluid in an edematous patient) Considerations: - Daily weights early in the morning after voiding but before he or she has eaten or defecated I

204. 1 Replacement of Fluid and Electrolytes General Principles: - Either by oral intake (healthiest way), tube feeding, intravenous infusion, and/or total parenteral nutrition - Normal saline solution and plain water should also be given by slow drip to replace daily fluid loss - IV administration per doctor’s orders - Fluid replacement considerations: * Most effective when apportioned over 24 hr period (Better regulation, ↓potential for calculi formation and subsequent renal damage, ↓potential for circulatory overload which may cause in fluid and electrolyte shifts) * Administer concentrated solutions of Na, Glucose or protein because they require body fluids for dilution * Consider the size of the patient (small adult has less fluid in each compartment, especially in the intravascular compartment) - Promote oral intake as appropriate * Caution with coffee, tea, and some colas I

205. * small amount at frequent intervals is more useful than a large amount presented less often * Always give consideration to cultural and aesthetic aspects of eating - Give mouth care to a dehydrated patient before and after meals and before bedtime (Xerostomia may lead to disruption of tissues in the oral cavity) - Avoid irritating foods - Stimulation of saliva may be aided by hard candy or chewing gum or carboxymethylcellulose (artificial saliva) - Keep lips moist and well lubricated - Give salty broth or soda crackers for sodium replacement and tea or orange juice for potassium replacement as appropriate. Bananas, citrus fruits and juices, some fresh vegetables, coffee, and tea are relatively high in potassium and low in sodium. Milk, meat, eggs, and nuts are high in protein, sodium and potassium. - Offer milk for patients with draining fistulas from any portion of the GI tract. Lactose intolerance is not necessarily a contraindication (Lactase enzyme preparations are available) - Increase usual daily requirement of foods when losses must be restored, as tolerated I

206. * Patients with cardiac and renal impairments are instructed to avoid foods containing high levels of sodium, potassium and bicarbonate - Administer replacement solutions through tube feeding as is * Either water, physiologic solution of NaCl, high protein liquids, or a regular diet can be blended, diluted and given by gavage * The water content in the tube feeding needs to be increased if: 1 the patient complains of thirst 2 the protein or electrolyte content of the tube feeding is high 3 the patient has fever or disease causing an increased metabolic rate 4 UO is concentrated 5 signs of water deficit develop - Administer parenteral fluids as necessary I

207. * Types of solutions - D5W (hypotonic) is given short-term for hyponatremia - D5NSS may be given depending on the serum levels of sodium and vascular volume + KCl to meet normal intake needs and replace losses for hyponatremia - Dextrose 5% in 0.2% normal saline is generally used as a maintenance fluid - Dextrose 5% in ½ normal saline is generally used as a replacement solution for losses caused by gastrointestinal drainage - PNSS is given primarily when large amounts of sodium have been lost and for patients with hyponatremia - LRS is also isotonic because it remains in the extracellular space - Fructose or 10-20% glucose in distilled water are hypertonic solutions and may partially meet body needs for CHOs - Dextran (commonly-used plasma expander) increases plasma volume by increasing oncotic pressure. May cause prolonged bleeding time and is CI in patients with renal failure, bleeding disorders, or severe CHF I

208. * Administration - The rate should be regulated according to the patient’s needs and condition per doctor’s orders - Monitor UO carefully. Refer marked decreases! - Verify orders for potassium administration in patients with renal failure and untreated adrenal insufficiency - Usual rate for fluid loss replacement: 3ml/min - Recognize signs of pulmonary edema (bounding pulse, engorged peripheral veins, hoarseness, dyspnea, cough, and rales) that can result from ↑IV rate - If infiltration occurs, the infusion should be stopped immediately and relocated. Peripheral IV sites are generally rotated every 72 hours - For dextran and other plasma expanders, observe for anaphylactic reaction (apprehension, dyspnea, wheezing, tightness of chest, angioedema, itching, hives and hypotension). If this happens, switch infusion to nonprotein solution and run at KVO rate, notify physician and monitor VS - Pronounced and continued thirst despite administration of fluids is not normal and should be reported (may indicate DM or hypercalcemia) I

209. I * Patient/Family Education - Include the signs and symptoms of water excess in discharge instructions - With drug therapy, instruct patient and family regarding correct method of administration, correct dose, and therapeutic and adverse effects - Instruct to read labels for nutritional content * For K restriction: avoid organ meats, fresh and dried fruits, and salt substitutes - Skin assessment and care, positioning techniques for patients with mobility restrictions

210. E * Achievement of outcomes is successful in disturbances in fluid and electrolyte balance: 1 Maintains functional fluid volume level with adequate UO, VS within the patient’s normal limits, sp gr of urine within 1.003-1.035, moist mucous membranes, stable weight, Intake=output, elastic skin turgor, and no edema 2 States possible causes of imbalance and plan to prevent recurrence of imbalances 3 Reports a decrease or absence of symptoms causing discomfort

211. Fluids and Electrolytes Acid-base balance

212. DRAWING ARTERIAL BLOOD GASES ALLEN’S TEST ARTERIAL PUNCTURE

213. NORMAL ACID-BASE BALANCE Definition and Implications Normal Value Parameter Partial pressure of oxygen in arterial blood (decreases with age) In adults < 60 years: 60-80 mmHg = mild hypoxemia 40-60 mmHg = moderate hypoxemia < 40 mmHg = severe hypoxemia 80-100 Hg PaO2 Identifies whether there is acidemia or alkalemia: pH<7.35 = acidosis; pH>7.45 = alkalosis 7.35-7.45 pH Partial pressure of CO2 in the arterial blood: PCO2<35 mmHg = respiratory alkalosis PCO2>45 mmHg = respiratory acidosis 35-45 mmHg PaCO2 Estimated HCO3 concentration after fully oxygenated arterial blood has been equilibrated with CO2 at a PCO2 of 40 mmHg at 38C; eliminates the influence of respiration on the plasma HCO3 concentration 22-26 mEq/L Standard HCO3

215. BASIC REGULATION OF ACID-BASE BALANCE CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3 Kidney Lungs The lungs help control acid-base balance by blowing off or retaining CO2. The kidneys help regulate acid-base balance by excreting or retaining HCO3

216. TYPES OF ACID-BASE DISTURBANCES Depression of the central nervous system, as evidenced by disorientation followed by coma ACIDOSIS Overexcitability of the nervous system; muscles may go into a state of tetany and convulsioons ALKALOSIS

218. EXPECTED DIRECTIONAL CHANGES WITH ACID-BASE IMBALANCES HCO3 PCO2 pH CONDITION Normal ↑ ↑ ↑ ↑ ↑ ↓ ↓ Normal Respiratory Acidosis Uncompensated Partly Compensated Compensated Normal ↓ ↓ ↓ ↓ ↓ ↑ ↑ Normal Respiratory Alkalosis Uncompensated Partly Compensated Compensated ↓ ↓ ↓ Normal ↓ ↓ ↓ ↓ Normal Metabolic Acidosis Uncompensated Partly Compensated Compensated ↑ ↑ ↑ Normal ↑ ↑ ↑ ↑ Normal Metabolic Alkalosis Uncompensated Partly Compensated Compensated

220. Compensation

221. RESPIRATORY ACIDOSIS: CARBONIC ACID EXCESS Damage to the respiratory center in the medulla, drug or narcotic use, obstruction of respiratory passages, respiratory and respiratory muscle disorders Decrease in the rate of pulmonary ventilation Increase in the concentration of CO2, carbonic acid, and hydrogen ions RESPIRATORY ACIDOSIS Potassium moves out of the cells HYPERKALEMIA VENTRICULAR FIBRILLATION

223. NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS ASSESSMENT * Health Hx: complaints of headache, confusion, lethargy, nausea, irritability, nausea, irritability, anxiety, dyspnea, and blurred vision, preexisting conditions * Physical Examination: lethargy to stupor to coma, tachycardia, hypertension, cardiac dysrhythmias, airway patency NURSING DIAGNOSES include but are not limited to: Diagnostic TitlePossible Etiologic Factors 1 Impaired gas exchange Hypoventilation 2 Disturbed thought processes Central nervous system depression 3 Anxiety Hypoxia, hospitalization 4 Risk for ineffective family Illness of a family member coping 5 Ineffective airway clearance Hypoventilation, secretions 6 Ineffective breathing pattern Hypoventilation, dyspnea

224. NURSING MANAGEMENT OF RESPIRATORY ACIDOSIS EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will maintain airway patency and adequate breathing rate and rhythm will return of ABGs to patient’s normal level 2 Will be alert and oriented to time, place, and person, or to his or her normal baseline level of consciousness 3 Will cope with anxiety 4 Will exhibit effective coping and awareness of effective support systems 5 Will have secretions that are normal for self in amount and can be raised 6 Will maintain adequate rate and depth of respirations using pursed lip and other breathing techniques when necessary (as in the patient with COPD)

225. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS INTERVENTIONS 1 Supporting effective gas exchange - Provide a position of comfort to allow ease of respiration - Obtain and monitor ABG results and VS. Refer accordingly - Provide and monitor supplemental oxygen as ordered - Turn the patient q2 and PRN - Provide pulmonary hygiene PRN - Maintain adequate hydration - Provide comfort measures such as mouth care - Assist with ADLs - Instruct patient regarding coughing and deep breathing and management of disease condition, especially COPD 2 Coping with disturbed thought processes - Do frequent neurologic assessments - Monitor and document person’s baseline LOC frequently

226. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS - Reorient as necessary by providing calendars, clocks, etc. 3 Relieving anxiety - Provide a calm, relaxed environment - Give clear, concise explanations of treatment plans - Encourage expression of feelings - Provide support and information to patient and family - Teach relaxation techniques - Assist the patient to identify coping mechanisms to deal with anxiety and stress 4 Enhancing coping mechanisms - Provide support and information to family members about the patient’s ongoing condition - Reassure them that there is a physiologic cause for the patient’s behavior

227. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS - Encourage questions and open communication 5 Promote airway clearance - Implement regular breathing and coughing exercises - Do suctioning as necessary - Maintain good hydration - Do chest physiotherapy as appropriate 6 Promoting an effective breathing pattern - Maintain alveolar ventilation - Teach the patient proper breathing techniques as well as panic control breathing

228. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1a. Demonstrates improved ventilation and oxygenation 1b Has vital signs, ABGs, and cardiac rhythm within own normal range 2 Returns to baseline LOC 3 Reports reduced anxiety 4 Family uses adequate coping mechanisms 5 Is able to raise secretions on own 6 Demonstrate effective breathing techniques

229. RESPIRATORY ALKALOSIS: CARBONIC ACID DEFICIT Anxiety, hysteria, fever, hypoxia, pain, pulmonary disorders, lesions affecting the respiratory center in the medulla, brain tumor, encephalitis, meningitis, hyperthyroidism, gram-negative sepsis Hyperventilation: Excessive pulmonary ventilation Decrease in hydrogen ion concentration RESPIRATORY ALKALOSIS

231. NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS ASSESSMENT * Health Hx: anxiety, shortness of breath, muscle cramps or weakness, palpitations, panic, dyspnea * Physical Examination: light-headedness, confusion as a result of cerebral hypoxia, hyperventilation, tachycardia or arrhythmia, muscle weakness, (+) Chvostek’s sign or Trousseau’s sign indicating a low ionized serum calcium level secondary to hyperventilation and alkalosis, hyperactive deep tendon reflexes, unsteady gait, muscle spasms to tetany, agitation, psychosis, seizures in extreme cases, decreased potassium levels NURSING DIAGNOSES include but are not limited to: Diagnostic TitlePossible Etiologic Factors 1 Anxiety Stress, fear 2 Ineffective breathing pattern Hyperventilation, anxiety 3 Disturbed thought processes CNS excitability; irritability 4 Risk for injury Change in LOC, and potential for seizures

232. NURSING MANAGEMENT OF RESPIRATORY ALKALOSIS EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will report decreased anxiety; verbalizes methods to cope with anxiety 2 Will return to normal respiratory rate and rhythm or at least decreased hyperventilation, with return to baseline ABGs 3 Will exhibit reorientation to person, place, and time as per patient’s baseline 4 Will be free from injury INTERVENTIONS 1 Allay anxiety - Give antianxiety medications as ordered - Have patient breath into a paper bag - Teach relaxation techniques when initial anxiety attack is over

233. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS INTERVENTIONS 2 Promoting an Effective Breathing Pattern - Encourage the patient to slow his or her RR - Maintain a calm and comforting attitude - Position the patient to promote maximal ease of inspiration - Assist the patient with relaxation techniques 3 Coping with Disturbed Thought Processes - Do frequent reorientation - Encourage family to participate in patient’s care - Use simple, direct statements or directions - Allow the patient adequate time to respond 4 Preventing injuries - Perform neurologic assessment frequently and document - Institute safety and seizure precautions - Assess frequently for muscle strength and coordination

234. NURSING MANAGEMENT OF PATIENT WITH RESPIRATORY ACIDOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1 Reports reduction in anxiety levels 2a Demonstrates effective normal breathing patterns 2b Has ABG results within patient’s normal baseline 3 Returns to normal baseline LOC and orientation level 4 Remains free from injury; no seizure activity

235. METABOLIC ACIDOSIS: BICARBONATE DEFICIT Increased acid production, uncontrolled diabetes mellitus, alcoholism, starvation, renal acidosis, lactic acidosis, increased acid ingestion, ethanol, salicylates, loss of bicarbonate, severe diarrhea, intestinal fistulas, adrenal insufficiency, hypoparathyroidism Excess organic acids are added to body fluids or bicarbonate is lost Decrease in bicarbonate concentration METABOLIC ACIDOSIS

237. NURSING MANAGEMENT OF METABOLIC ACIDOSIS ASSESSMENT * Health Hx: anorexia, nausea, vomiting, abdominal pain, headache, thirst if the patient is dehydrated * Physical Examination: confusion, hyperventilation, warm, flushed skin, bradycardia and other dysrhythmias, decreasing LOC, nausea, vomiting, diarrhea, Kussmaul respirations, and acetone breath, especially if acidosis is due to ketoacidosis. Symptoms may progress to coma if untreated NURSING DIAGNOSES include but are not limited to: Diagnostic TitlePossible Etiologic Factors 1 Disturbed thought processes Secondary to CNS depression 2 Decreased cardiac output Dysrhythmias 3 Risk for injury Secondary to altered mental state 4 Risk for imbalanced fluid Diarrhea, renal failure volume

238. NURSING MANAGEMENT OF METABOLIC ACIDOSIS EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will return to usual baseline LOC 2 Will return to normal baseline parameters for vital signs with improved CO and decreased or resolved dysrhythmias 3 Will remain in a safe, secure environment without injury 4 Will maintain fluid and electrolyte balance and stable renal status INTERVENTIONS 1 Coping with disturbed thought processes - Monitor LOC and reorient as necessary - Monitor VS, esp. RRR, BP, and T - Monitor ABGs to assess the effects of treatment - Institute cardiac monitoring as ordered

239. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS 2 Supporting cardiac output - Monitor VS, MIO, and fluid and electrolyte balance - Institute cardiac monitoring to evaluate cardiac status 3 Promoting safety - Provide a safe, secure and monitored environment - Institute safety precautions 4 Promoting return of fluid and electrolyte balance - Monitor MIO - Administer medications per medical order

240. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ACIDOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1 Exhibits baseline-level consciousness and orientation 2 Returns to normal baseline parameters for vital signs and Cardiac Output with cardiac dysrhythmias resolved 3 Remains free from injury 4 Maintains fluid and electrolyte balance and stable renal function

241. METABOLIC ALKALOSIS: BICARBONATE EXCESS Loss of stomach acid, gastric suctioning, persistent vomiting, excess alkali intake, intestinal fistulas, hypokalemia, Cushing’s syndrome or aldosteronism, potassium-diuretic therapy Excessive amounts of acid substance and hydrogen ions are lost from the body or large amounts of bicarbonate or lactate are added orally or IV Excess of base elements METABOLIC ALKALOSIS

243. NURSING MANAGEMENT OF METABOLIC ALKALOSIS ASSESSMENT * Health Hx: Prolonged vomiting or nasogastric suctioning, frequent self-induced vomiting, muscle weakness, light- headedness, ingestion of large amounts of licorice or antacids, use of diuretics, muscle cramping, twitching, or tingling * Physical Examination: mental confusion, dizziness, changes in LOC, hyperreflexia, tetany, dysrhthmias, seizurees, respiratory failure, positive Chvostek’s or Trosseau’s sign if the patient has a low ionized serum calcium level, decreased hand grasps, generalized muscle weakness, decreased serum calcium or potassium level, impaired concentration, seizures, ECG changes consistent with hypokalemia NURSING DIAGNOSES include but are not limited to: Diagnostic TitlePossible Etiologic Factors 1 Disturbed thought processes CNS excitation 2 Decreased cardiac output Dysrhythmias and electrolyte imbalances 3 Risk for injury Muscle weakness, tetany, confusion and possible seizures 4 Risk for imbalanced fluid Nasogastric drainage, diuretic therapy volume fistula

244. NURSING MANAGEMENT OF METABOLIC ALKALOSIS EXPECTED PATIENT OUTCOMES include but are not limited to: 1 Will return to usual baseline LOC and orientation 2 Will return to normal baseline parameters for vital signs with improved CO with resolution of electrolyte imbalances and decreased or resolved cardiac dysrhythmias 3 Will remain in a safe, secure environment without injury 4 Will maintain fluid and electrolyte balance INTERVENTIONS 1 Coping with disturbed thought processes - Monitor LOC and reorient as necessary - Monitor VS, esp. RRR, BP, and T - Monitor ABGs to assess the effects of treatment - Institute cardiac monitoring as ordered

245. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS 2 Supporting cardiac output - Monitor VS, MIO, and fluid and electrolyte balance - Institute cardiac monitoring to evaluate cardiac status 3 Promoting safety - Provide a safe, secure and monitored environment - Institute safety precautions 4 Promoting return of fluid and electrolyte balance - Monitor MIO - Administer medications per medical order

246. NURSING MANAGEMENT OF PATIENT WITH METABOLIC ALKALOSIS EVALUATION. Achievement of outcomes is successful when the patient: 1 Manifests mental status has returned to baseline 2 Is free from cardiac dysrhythmias 3 Remains free from injury 4 Maintains fluid balance at baseline level

247. CRITICAL THINKING EXERCISES A 32-year-old administrative assistant comes to the urgent care center with a 72-hour history of vomiting secondary to influenza. She is lethargic and states, “My muscles are twitching.” Her RR is 18/min and HR is 110 bpm, T=100.4F. Her blood pressure is 110/68 which she states “is about normal for me.” Her ABG values are as follows: pH: 7.57 PaO2: 92 PaCO2: 41 HCO3: 36 Describe her acid-base status, probable cause for the imbalance and treatment