Presentation is loading. Please wait.

Presentation is loading. Please wait.

Fluid and Electrolytes, Balance and Disturbances

Similar presentations


Presentation on theme: "Fluid and Electrolytes, Balance and Disturbances"— Presentation transcript:

1 Fluid and Electrolytes, Balance and Disturbances
Larry Santiago, MSN, RN

2 Fluid and Electrolytes
60% of body consists of fluid Intracellular space [2/3] Extracellular space [1/3] Electrolytes are active ions: positively and negatively charged

3 Fluid and Electrolytes 2

4 Regulation of Body Fluid Compartments
Osmosis is the diffusion of water caused by fluid gradient

5 Regulation of Body Fluid Compartments 2
Tonicity is the ability of solutes to cause osmotic driving forces

6 Regulation of Body Fluid Compartments 3
Diffusion is the movement of a substance from area of higher concentration to one of lower concentration “Downhill Movement”

7 Regulation of Body Fluid Compartments 4
Filtration is the movement of water and solutes from an area of high hydrostatic pressure to an area of low hydrostatic pressure

8 Regulation of Body Fluid Compartments 5
Osmolality reflects the concentration of fluid that affects the movement of water between fluid compartments by osmosis

9 Regulation of Body Fluid Compartments 6
Osmotic pressure is the amount of hydrostatic pressure needed to stop the flow of water by osmosis

10 Sodium-Potassium Pump
Sodium concentration is higher in ECF than ICF Sodium enters cell by diffusion Potassium exits cell into ECF

11 Gains and Losses Water and electrolytes move in a variety of ways
Kidneys Skin Lungs GI tract

12 Fluid Volume Disturbances
Fluid Volume Deficit (Hypovolemia)

13 Fluid Volume Deficit Mild – 2% of body weight loss
Moderate – 5% of body weight loss Severe – 8% or more of body weight loss

14 Fluid Volume Deficit Pathophysiology – results from loss of body fluids and occurs more rapidly when coupled with decreased fluid intake

15 Fluid Volume Deficit 2 Clinical manifestations Acute weight loss
Decreased skin turgor

16 Fluid Volume Deficit 3 - Oliguria - Concentrated urine
- Postural hypotension - Weak, rapid, heart rate - Flattened neck veins - Increased temperature - Decreased central venous pressure

17 Fluid Volume Deficit 4 Gerontologic considerations

18 Nursing Diagnosis Fluid volume Deficit r/t
Insufficient intake, vomiting, diarrhea, hemorrage m/b dry mucous membranes, low BP, HR , BUN 28, Na 152, urine dark amber; Intake 200mL/Output 450mL over 24 hours Goal: Client will have adequate fluid volume within 24 hours AEB: Moist tongue, mucous membranes, BNL WNL, HR WNL, BUN between 8-20, Na , Urine clear yellow, balanced I/O

19 Fluid Volume Deficit 5 Nursing management Restore fluids by oral or IV
Treat underlying cause Monitor I & O at least every 8 hours Daily weight Vital signs Skin turgor Urine concentration

20 Fluid Volume Disturbances 2
Fluid Volume Excess (Hypervolemia)

21 Fluid Volume Excess Pathophysiology – may be related to fluid overload or diminished function of the homeostatic mechinisms responsible for regulating fluid balance Contributing factors – CHF, renal failure, cirrhosis

22 Fluid Volume Excess 2 Clinical manifestations – edema, distended neck veins, crackles, tachycardia, increased blood pressure, increased weight

23 Nursing Diagnosis and Goal
Fluid volume excess r/t CHF, excess sodium intake, renal failure AEB: Weight gain of 6 lb. in 24 hours; lungs with crackles in bases bilaterally; 2+ edema in ankles bilaterally Goal: Client will have normal fluid volume within 48 hours AEB: Decreased weight of 1 lb. per day, lung sounds clear in all fields, ankles without edema

24 Fluid Volume Excess 3 Nursing management Preventing FVE
Detecting and Controlling FVE Teaching patients about edema

25 Electrolyte Imbalances
Sodium! Normal range – 135 to 145 mEq/L Primary regulator of ECF volume (a loss or gain of sodium is usually accompanied by a loss or gain of water)

26 Hyponatremia Sodium level less than 135 mEq/L
May be caused by vomiting, diarrhea, sweating, diuretics, etc.

27 Hyponatremia 2 Clinical manifestations Poor skin turgor Dry mucosa
Decreased saliva production Orthostatic hypotension Nausea/abdominal cramping Altered mental status

28 Hyponatremia 3 Medical management Sodium Replacement Water Restriction

29 Hyponatremia 4 Nursing Management
- Detecting and controlling hyponatremia - Returning sodium level to normal

30 Critical Thinking Exercise: Nursing Management of the Client with Hyponatremia
Situation: An 87 year old man was admitted to the acute care facility for gastroenteritis, 2 day duration. He is vomiting, has severe, watery diarrhea and is c/o abd cramping. His serum electrolytes are consistent with hyponatremia r/t excessive sodium loss.

31 Critical Thinking Exercise: Nursing Management of the Client with Hyponatremia 2
1. What is the relationship between vomiting, diarrhea, and hyponatremia? 2. What s/s should the client be monitored for that indicate the presence of sodium deficit? 3. In addition to examining the client’s serum electrolyte findings, how will the nurse know when the client’s sodium level has returned to normal?

32 Hypernatremia Sodium level is greater than 145 mEq/L
- Can be caused by a gain of sodium in excess of water or by a loss of water in excess of sodium

33 Hypernatremia 2 Pathophysiology
Fluid deprivation in patients who cannot perceive, respond to, or communicate their thirst Most often affects very old, very young, and cognitively impaired patients

34 Hypernatremia 3 Clinical manifestations Thirst Dry, swollen tongue
Sticky mucous membranes Flushed skin Postural hypotension

35 Hypernatremia 4 Medical Management Nursing Management
- Preventing Hypernatremia - Correcting Hypernatremia

36

37 Critical Thinking Exercise: Nursing Management of the Client with Hypernatremia
Situation: A 47 year old woman was taken to the ER after she developed a rapid heart rate and agitation. Physical assessment revealed dry oral mucous membranes, poor skin turgor, and fever of orally. The client’s daughter stated her mother had been very hungry recently and drinking more fluids than usual. Suspecting DM, the practitioner obtained serum electrolytes and glucose levels, which revealed serum sodium of 163 mEq/L and serum glucose of 360 mg/dL.

38 Critical Thinking Exercise: Nursing Management of the Client with Hypernatremia 2
1. Interpret the client’s lab data. 2. Why are clients with DM prone to the development of hypernatremia? 3. What precautions should the nurse take when caring for the client with hypernatremia? 4. List 4 food items this client should avoid and why. 5. Identify 3 meds that could have an increased effect on the client’s sodium level.

39 All About Potassium Major Intracellular electrolyte
98% of the body’s potassium is inside the cells Influences both skeletal and cardiac muscle activity Normal serum potassium concentration – 3.5 to 5.5 mEq/L.

40 Hypokalemia Serum Potassium below 3.5 mEq/L Causes:
Diarrhea, diuretics, poor K intake, stress, steroid administration

41 Hypokalemia 2 Clinical manifestations:
Muscle weakness, cardiac arrythmias, increased sensitivity to digitalis toxicity, fatigue, EKG changes (like ST elevation)

42 SUCTION Skeletal muscle weakness U wave (EKG changes)
Constipation, ileua Toxicity of digitalis glycosides Irregular, weak pulse Orthostatic hypotension Numbness (paresthesia)

43 Hypokalemia 3 Nursing interventions: Encourage high K foods
Monitor EKG results Dilute KCl! – can cause cardiac arrest if given IVP

44 Hypokalemia 4 Administering IV Potassium
Should be administered only after adequate urine flow has been established Decrease in urine volume to less than 20 mL/h for 2 hours is an indication to stop the potassium infusion IV K+ should not be given faster than 20 mEq/h

45 Critical Thinking Exercise: Nursing Management of the Client with Hypokalemia
Situation: A 69 year old man has a history of CHF controlled by Digoxin and Lasix. Two weeks ago he developed diarrhea, which has persisted in spite of his taking OTC antidiarrheal meds. His partner transported him to the ER when she found him lethargic and confused. Initial assessment of the client reveals heart rate at 86 bpm, respiratory rate 10, and blood pressure 102/56 mmHg.

46 Critical Thinking Exercise: Nursing Management of the Client with Hypokalemia 2
1. An electrolyte panel shows the client’s serum potassium is 2.9 mEq/L. Does the nurse have cause to be concerned about the client’s serum potassium? Why or why not? 2. What data supports the presence of hypokalemia in this client? 3. What, if anything, should the nurse do? 4. What foods should the client be advised to eat that are high in potassium?

47 Hyperkalemia Serum Potassium greater than 5.5 mEq/L
More dangerous than hypokalemia because cardiac arrest is frequently associated with high serum K+ levels

48 Hyperkalemia 2 Causes: - Decreased renal potassium excretion as seen with renal failure and oliguria - High potassium intake - Renal insufficiency - Shift of potassium out of the cell as seen in acidosis

49 Hyperkalemia 3 Clinical manifestations:
Skeletal muscle weakness/paralysis EKG changes – such as peaked T waves, widened QRS complexes Heart block

50 Hyperkalemia 4 Medical/Nursing Management:
Monitor EKG changes – telemetry Administer Calcium solutions to neutralize the potassium Monitor muscle tone Give Kayexelate Give Insulin and D50W

51 Calcium More than 99% of the body’s calcium is located in the skeletal system Normal serum calcium level is 8.5 to 10mg/dL Needed for transmission of nerve impulses Intracellular calcium is needed for contraction of muscles

52 Calcium 2 Extracellular needed for blood clotting
Needed for tooth and bone formation Needed for maintaining a normal heart rhythm

53 Hypocalcemia Serum Calcium level less than 8.5 mEq/L

54 Hypocalcemia 2 Causes Vitamin D/Calcium deficiency
Primary/surgical hyperparathyroidism Pancreatitis Renal failure

55 Hypocalcemia 3 Clinical Manifestations
- Tetany and cramps in muscles of extremities Definition – A nervous affection characterized by intermitten tonic spasms that are usually paroxysmal and involve the extremities

56 Hypocalcemia 4 Trousseau’s sign – carpal spasms

57 Hypocalcemia 5 Chvostek’s sign – cheek twitching

58 Hypocalcemia 6 Seizures, mental changes

59 Hypocalcemia 7 EKG shows prolonged QT intervals

60 Hypocalcemia 8 Medical/Nursing management
IV/PO Calcium Carbonate or Calcium Gluconate Encourage increased dietary intake of Calcium Monitor neurlogical status Establish seizure precautions

61 Hypercalcemia Serum Calcium level greater than 10.5 mEq/L

62 Hypercalcemia 2 Causes: Hyperparathyroidism Prolonged immobilization
Thiazide diuretics Large doses of Vitamin A and D

63 Hypercalcemia 3 Clinical manifestations:
Muscle weakness, nausea and vomiting Lethargy and confusion Constipation Cardiac Arrest (in hypercalcemic crisis, level 17mg/dL or higher)

64 Hypercalcemia 4 Medical/Nursing Management Eliminate Calcium from diet
Monitor neurological status Increase fluids (IV or PO) Calcitonin

65 Calcitonin - used to lower serum calcium level
- useful for pts with heart disease or renal failure - reduces bone resorption - increases deposit of calcium and phosphorus in the bones - increases urinary excretion of calcium and phosphorus

66 Parathyroid pulls, calcitonin keeps
Parathyroid hormone pulls calcium out of the bone. Calcitonin keeps it there.

67 Magnesium Normal serum magnesium level is 1.5 to 2.5 mg/dL
Helps maintain normal muscle and nerve activity Exerts effects on the cardiovascular system, acting peripherally to produce vasodilation Thought to have a direct effect on peripheral arteries and arterioles

68 Hypomagnesemia Serum Magnesium level less than 1.5 mEq/L

69 Hypomagnesemia Causes Chronic Alcoholism
Diarrhea, or any disruption in small bowel function

70 Hypomagnesemia 2 TPN - Diabetic ketoacidosis

71

72 Hypomagnesemia 4 Clinical manifestations Neuromuscular irritability
Positive Chvostek’s and Trousseau’s sign EKG changes with prolonged QRS, depressed ST segment, and cardiac dysrhythmias May occur with hypocalcemia and hypokalemia

73 STARVED Starved – possible cause of hypomagnesemia Seizures Tetany
Anorexia and arrhythmias Rapid heart rate Vomiting Emotional lability Deep tendon reflexes increased

74 Hypomagnesemia 5 Medical/Nursing management
IV/PO Magnesium replacement, including Magnesium Sulfate Give Calcium Gluconate if accompanied by hypocalcemia Monitor for dysphagia, give soft foods Measure vital signs closely

75 Hypomagnesemia 6 Foods high in Magnesium: - Green leafy vegetables

76 Hypomagnesemia 7 Nuts Legumes

77 Hypomagnesemia 8 Seafood Chocolate

78 Hypermagesemia Serum Magnesium level greater than 2.5 mEq/L

79 Hypermagnesemia 2 Causes Renal failure Untreated diabetic ketoacidosis
Excessive use of antacids and laxatives

80 Hypermagnesemia 3 Clinical manifestations Flushed face and skin warmth
Mild hypotension

81 Hypomagnesemia 4 Heart block and cardiac arrest
Muscle weakness and even paralysis

82 RENAL Reflexes decreased (plus weakness and paralysis)
ECG changes (bradycardia and hypotension) Nausea and vomiting Appearance flushed Lethargy (plus drowsiness and coma)

83 Hypermagnesemia 5 Medical/Nursing management Monitor Mg levels
Monitor respiratory rate Monitor cardiac rhythm Increase fluids IV calcium for emergencies

84 Phosphorus Normal serum phosphorus level is 2.5 to 4.5 mg/dL
Essential to the function of muscle and red blood cells, maintanence of acid-base balance, and nervous system Phosphate levels vary inversely to calcium levels High Calcium = Low Phosphate

85 Hypophosphatemia Serum Phosphorus level less than 2.5 mEq/L

86 Hypophosphatemia 2 Causes
Most likely to occue with overzealous intake or administration of simple carbohydates Severe protein-calorie malnutrition (anorexia or alcoholism)

87 Hypophosphatemia 3 Clinical manifestations Muscle weakness
Seizures and coma Irritability Fatigue Confusion Numbness

88 Hypophosphatemia 4 Medical/Nursing management Prevention is the goal
IV Phosphorus for severe Prevention of infection Monitor phosphorus levels Increase oral intake of phosphorus rich foods

89 Hypophosphatemia 5 Foods rich in Phosphorus: Milk and milk products
Organ meats Nuts Fish

90 Hypophosphatemia 6 Poultry Whole grains

91 Hyperphosphatemia Serum Phosphorus level greater than 4.5 mEq/L Causes
Renal failure Chemotherapy Hypoparathyroidism High phosphate intake

92 Hyperphosphatemia 2 Clinical manifestations Tetany Muscle weakness
Similar to Hypocalcemia because of reciprocal relationship

93 Hyperphosphatemia 3 Medical/Nursing management Treat underlying cause
Avoid phosphorus rich foods

94 Nursing Management in Cancer Care
Larry Santiago, MSN, RN

95 7 Warning Signs of Cancer
Change in bowel or bladder habits A sore that does not heal Unusual bleeding or discharge Thickening or lump in breast or elsewhere Indigestion or difficulty in swallowing Obvious change in a mole or wart Nagging cough or hoarseness

96 Benign Tumors Benign – Not recurrent or progressive. Opposite of malignant

97 Pathophysiology of the Malignant Process
Characteristics of Malignant Cells All cancer cells share some common cellular characteristics Cell membrane of malignant cells contain proteins called tumor-specific antigens, such as carcinoembryonic antigen and PSA

98 Pathophysiology 2 Invasion – growth of the primary tumor into the surrounding host tissues Metastasis – dissemination or spread of malignant cells from the primary tumor to distant sites

99 Detection and Prevention of Cancer
Primary Prevention Use teaching and counseling skills to encourage patients to partipate in cancer prevention and promote a healthy lifestyle

100 Detection and Prevention of Cancer 2
Secondary Prevention Examples – breast and testicular self-examination, Pap smear

101 Detection and Prevention of Cancer 3
Tumor Staging and Grading Staging determines size of tumor and existence of metastasis Grading classifies tumor cells by type of tissue

102

103

104 Cancer Management- Cure, Control, or Palliation
Surgery Radiation Chemotherapy

105

106 Chemotherapy problems
Myelosuppression Pulmonary or cardiac toxicity Nausea and vomiting Extravasation Hypersensitivity reactions Neuropathy Pain at the injection site Flulike syndrome Hyperglycemia

107 Cancer Management- Cure, Control, or Palliation
Bone marrow transplantation

108 Nursing Process: The Patient with Cancer
Risk for Infection Impaired Skin Integrity Impaired Oral Mucous Membrane: Stomatitis Imbalanced Nutrition: Less Than Body Requirements Fatigue Chronic Pain

109 Leukemia A neoplastic proliferation of one particular cell type (granulocytes, monocytes, lymphocytes, or megakaryocytes) Common feature is an unregulated proliferation of WBCs in the bone marrow

110

111 Acute leukemia Progresses rapidly; characterized by ineffective, immature cells in the bone marrow pushing out the normal cells. Acute myeloid leukemia (AML)--adults Acute lymphocytic leukemia (ALL)--children Signs and symptoms: Pallor, headache, fatigue, malaise, loss of appetite, weight loss, tachycardia, shortness of breath, petechiae, ecchymosis, splenomegaly, and bone tenderness.

112 Acute myelogenous leukemia (AML)
Normally, myelogenous line of cells mature into neutro-phils, monocytes, eosinophils, RBCs, and platelets. AML develops when cells commit to one type, typically neutrophils. Diagnosis: Bone marrow biopsy Prognosis: Favorably affected by age under 60 years, spontaneous rather than secondary leukemia, WBC less than 10,000/mm3 and remission after one round of chemotherapy.

113 AML treatment options Induction chemotherapy Goal is remission
Cytosine arabinoside and an anthracycle Postinduction therapy (consolidation) Goal is to prevent relapse after remission, but effective in only 25% to 35% of patients. High-dose cytarabine has improved duration of first remission in young patients with AML. Options: Standard chemotherapy, autologous stem cells, or human-leukocyte-antigen (HLA) matched sibling or donor (allogenic).

114 Acute lymphocytic leukemia (ALL)
Rapidly developing immature lymphocytes crowd our normal cells Poor prognostic factors: High WBCs (> 25,000/mm3 at presentation), age over 50 years, and slow first remission (longer than 4 weeks). Treatment - Induction chemotherapy, administered in two phases, followed by maintenance therapy for up to 36 months. Goal is complete remission.

115 Chronic leukemia Progresses slowly and rarely affects people under age 20. Chronic myeloid leukemia (CML) strikes ages 40 to 50, more in males. Chronic lymphocytic leukemia (CLL) strikes after age 40 and is most common in older men.

116 Chronic myeloid leukemia (CML)
Too many neutrophils and the presence of the Philadelphia chromosome. Chronic phase follows an indolent course, mild symptoms, <10% blasts in the marrow. Accelerated phase characterized by spleen enlargement and progressive intermittent fevers, night sweats, and unexplained weight loss. 10% to 30% blasts and promyelocytes. It last 6 to 12 months. Blast phase characterized by transformation to a very aggressive acute leukemia. 30% blasts and premyelocytes; patients die in this phase.

117 CML treatment options Kinase inhibitor imatinib (Gleevec) is treatment of choice Interferon alpha reduces growth and division 55% to 60%. Hydroxyurea may prolong the chronic phase. Stem cell transplant--greatest risk of dying in the first 100 days.

118 Chronic lymphocytic leukemia (CLL)
Average survival is 2.5 years for advanced disease and 14 years for those with early-stage disease. Indolent disease characterized by lymphocytosis, lymphadenopathy and hepatosplenomegaly. Risk of death from infection as the disease advances.

119 CLL treatment options Standard chemotherapy, which can produce a remission not a cure and has harsh adverse reactions. Usually delayed till signs and symptoms appear. Chemotherapy, radiation, and Rituximab to enhance the response.

120 Lymphoma Neoplastic disease in which lymphocytes undergo malignant changes and produce tumors Classified as Hodgkin’s disease (accounts for 12% of lymphomas) and non-Hodgkin’s lymphoma (NHL) Hodgkin’s disease accounted for 5 % of all cancer diagnoses in 2005; 3% NHL

121 Stages of lymphoma Stage I – involves a single lymph node or localized involvement Stage II – involves two or more lymph node regions on the same side of the diaphragm Stage III – involves several lymph node regions on both sides of the diaphragm Stage IV – involves extralymphatic tissue, such as the bone marrow

122 Hodgkin’s treatment options
Radiation is treatment of choice for stage IA or IIA nonbulky (<9 cm) Hodgkin’s. Over 95% achieve complete remission and 90% survive beyond 20 years. Chemotherapy is appropriate for stage IIIB or IV, bulky disease. Standard ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) regimen is used.

123 Non-Hodgkin’s lymphoma (NHL)
Incidence has increased about 7% annually over 20 years, primarily older adults. Cause is unknown but increased risk: long-term immunosuppressant therapy, bone marrow transplant, inherited immune defects, rheumatoid arthritis, and prior Hodg-kin’s disease and treatment. Spread through the bloodstream.

124 NHL Treatment Options Radiation, chemotherapy, or both
Stem cell transplant for recurrent disease

125 Multiple Myeloma A malignant disease of the most mature form of B lymphocyte

126 Multiple Myeloma 2 Clinical Manifestations Bone pain Hypercalcemia
Renal failure Anemia Oral hemorrhage Fatigue, weakness

127 Assessment and Diagnostic Findings

128 Medical/Nursing Management

129


Download ppt "Fluid and Electrolytes, Balance and Disturbances"

Similar presentations


Ads by Google