1. Fluid & electrolytes balance and disturbances Dr.HELEN SHAJI, Ph.D (N)

2. WHY IS IT IMPORTANT FOR NURSES TO KNOW ABOUT FLUID & ELECTROLYTE BALANCE

3. INTRODUCTION: Water is found everywhere on earth including human body In an adult 60% of the weight is water Two third of the body’s water is found in the cell

4. DISTRIBUTION OF BODY FLUIDS: Body fluids are distributed in two distinct compartments: 1.Extracellular fluids[ECF] Which includes interstitial fluid & intravascular fluid 2.Intracellular fluids[ICF]

5. COMPOSITION OF BODY FLUIDS: The fluids circulating throughout the body in extracellular and intracellular fluid spaces contain 1.Electrolytes 2.Minerals 3.Cells

6. Fluid Volume Deficit (Hypovolemia, Isotonic Dehydration) Common Causes – Hemorrhage – Vomiting – Diarrhea – Burns – Diuretic therapy – Fever – Impaired thirst

7. THREE TYPES OF ECFVD Hyperosmolar fluid volume deficit - water loss is greater than the electrolyte loss Isosmolar fluid volume deficit – equal proportion of fluid and electrolyte loss Hypotonic fluid volume deficit – electrolyte loss is greater than fluid loss

8. Clinical Manifestations Signs/Symptoms – Weight loss – Thirst – Orthostatic changes in pulse rate and BP – Weak, rapid pulse – Decreased urine output – Dry mucous membranes – Poor skin turgor

9. Treatment/Interventions (FVD) Fluid Management – Diet therapy – Mild to moderate dehydration. Correct with oral fluid replacement. – Oral rehydration therapy – Solutions containing glucose and electrolytes. E.g., Pedialyte, Rehydralyte. – IV therapy – Type of fluid ordered depends on the type of dehydration and the clients cardiovascular status.

10. Nursing Implications Monitor postural heart rate and B.P when getting patients out of bed

11. Fluid Volume Excess Common Causes: – Congestive Heart Failure – Early renal failure – IV therapy – Excessive sodium ingestion – SIADH (Syndrome of Inappropriate secretion of Anti Diuretic Hormone) – Corticosteroid

12. Clinical Manifestations Signs/Symptoms – Increased BP – Bounding pulse – Venous distention – Pulmonary edema Dyspnea Orthopnea (diff. breathing when supine) crackles

13. Treatment/Interventions (FVE) Drug therapy – Diuretics may be ordered if renal failure is not the cause. Restriction of sodium and saline intake I/O Weight

14. More to consider? Age – Infants – Older adults Prior medical history – Acute illness – Chronic illness – Environmental factors – Diet – Lifestyle – Medications

15. Physical Assessment – Body systems – I/O – Weight – Labs

16. Electrolyte Imbalance

17. NORMAL VALUE Serum Sodium - 135 to 145 mEq/L Serum Potassium – 3.5 to 5.0 mEq/L Serum Calcium – 9 to 10.5 mEq/L Serum Phosphate – 2.5 to 4.5 mEq/L Serum Magnesium – 1.4 to 2 mEq/L

18. Hypokalemia (<3.5mEq/L) Pathophysiology – – Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive to normal stimuli

19. Hypokalemia (<3.5mEq/L) Contributing factors: – Diuretics – Shift into cells – Digitalis – Water intoxication – Corticosteroids – Diarrhea – Vomiting

21. Hypokalemia (<3.5mEq/L) Interventions – Assess and identify those at risk – Encourage potassium-rich foods – K+ replacement (IV or PO) – Monitor lab values – Stop potassium-wasting diuretics – Treat underlying cause

22. Potassium- Rich Foods Vegetables Avocado Raw carrot Baked potato Raw tomato Spinach Meat and Fish Beef Cod pork Fruits Dried fruits Banana Apricot Orange Beverages Milk Orange juice Apricot nectar

23. Hyperkalemia (>5.0mEq/L) Pathophysiology – An increase in K+ causes increased excitability of cells.

24. Hyperkalemia (>5.0mEq/L) Contributing factors: – Increase in K+ intake – Renal failure – K+ sparing diuretics (eg: Tab. Aldactone) – Shift of K+ out of the cells

26. Hyperkalemia (>5.0mEq/L) Interventions – Need to restore normal K+ balance: – Eliminate K+ administration – Inc. K+ excretion Lasix Kayexalate (Polystyrene sulfonate) – Infuse glucose and insulin – Cardiac Monitoring

27. Hyponatremia (<135mEq/L) Contributing Factors – Excessive diaphoresis – Wound Drainage – NPO – CHF – Low salt diet – Renal Disease – Diuretics

28. Hyponatremia (<135mEq/L) Assessment findings: – Neuro - Generalized skeletal muscle weakness. Headache / personality changes. – Resp.- Shallow respirations – CV - Cardiac changes depend on fluid volume – GI – Increased GI motility, Nausea, Diarrhea (explosive) – GU - Increased urine output

29. Hyponatremia (<135mEq/L) Interventions/Treatment – Restore Na levels to normal and prevent further decreases in Na. – Drug Therapy – (FVD) - IV therapy to restore both fluid and Na. If severe may see 2-3% saline. (FVE) – Administer osmotic diuretic (Mannitol) to excrete the water rather than the sodium. – Increase oral sodium intake and restrict oral fluid intake.

30. Hypernatremia (>145mEq/L) Contributing Factors – Hyperaldosteronism – Renal failure – Corticosteroids – Increase in oral Na intake – Na containing IV fluids – Decreased urine output with increased urine concentration

31. Hypernatremia (>145mEq/L) Contributing factors (cont’d): – Diarrhea – Dehydration – Fever – Hyperventilation

32. Hypernatremia (>145mEq/L) Assessment findings: – Neuro - Spontaneous muscle twitches. Irregular contractions. Skeletal muscle weakness. Diminished deep tendon reflexes – Resp. – Pulmonary edema – CV – Diminished CO. HR and BP depend on vascular volume.

33. Hypernatremia (>145mEq/L) GU – Dec. urine output. Inc. specific gravity Skin – Dry, flaky skin. Edema r/t fluid volume changes.

34. Hypernatremia (>145mEq/L) Interventions/Treatment – Drug therapy (FVD).45% NSS. If caused by both Na and fluid loss, will administer NaCL. If inadequate renal excretion of sodium, will administer diuretics. – Diet therapy Mild – Ensure water intake

35. Hypocalcemia (<9.0mEq/L) Contributing factors: – Dec. oral intake – Lactose intolerance – Dec. Vitamin D intake – End stage renal disease – Diarrhea

36. Hypocalcemia (<9.0mEq/L) Contributing factors (cont’d): Acute pancreatitis Hyperphosphatemia Immobility Removal or destruction of parathyroid gland

37. Hypocalcemia (<9.0mEq/L) Assessment findings: – Neuro –Irritable muscle twitches. Positive Trousseau’s sign. Positive Chvostek’s sign. – Resp. – Resp. failure d/t muscle tetany. – CV – Dec. HR., dec. BP, diminished peripheral pulses – GI – Increased motility. Increased Bowel Sounds, Diarrhea

38. Positive Trousseau’s Sign

39. TROUSSEAU’S SIGN Elicitation: Inflating a sphygmomanometer cuff above systolic blood pressure for several minutes Postitive response: Muscular contraction including flexion of the wrist and metacarpo phalangeal joints, hyperextension of the fingers, and flexion of the thumb on the palm, suggestive of neuromuscular excitability caused by hypocalcemia

40. Positive Chvostek’s Sign

41. CHVOSTEK’S SIGN Elicitation: Tapping on the face at a point just anterior to the ear and just below the zygomatic bone Postitive response: Twitching of the ipsilateral facial muscles, suggestive of neuromuscular excitability caused by hypocalcemia

42. Hypocalcemia (<9.0mEq/L) Interventions/Treatment – Drug Therapy Calcium supplements Vitamin D – Diet Therapy High calcium diet – Prevention of Injury Seizure precautions

43. Hypercalcemia Contributing factors: – Excessive calcium intake – Excessive vitamin D intake – Renal failure – Hyperparathyroidism – Malignancy – Hyperthyroidism

44. Hypercalcemia (>10.5mg/dL) Assessment findings: – Neuro – Disorientation, lethargy, coma, profound muscle weakness – Resp. – Ineffective resp. movement – CV - Inc. HR, Inc. BP., Bounding peripheral pulses, Positive Homan’s sign. Late Phase – Bradycardia, Cardiac arrest – GI – Dec. motility. Dec. BS. Constipation – GU – Inc. urine output. Formation of renal calculi

45. Hypercalcemia (>10.5mg/dL) Interventions/Treatment – Eliminate calcium administration – Drug Therapy – Isotonic NaCL (Inc. the excretion of Ca) – Diuretics – Calcium reabsorption inhibitors (Phosphorus) – Cardiac Monitoring

46. Hypophosphatemia (<2.5mg/L) Contributing Factors: – Malnutrition – Starvation – Hypercalcemia – Renal failure – Uncontrolled DM

47. Hypophosphatemia (<2.5mg/L) Assessment findings: Neuro – Irritability, confusion CV – Dec. contractility Resp. – Shallow respirations Hematologic – Inc. bleeding Dec. platelet aggregation

48. Hypophosphatemia (<2.5mg/L) Interventions – Treat underlying cause – Oral replacement with vit. D – IV phosphorus (Severe) – Diet therapy Foods high in oral phosphate

49. Hyperphosphatemia (>4.5mg/L) Causes few direct problems with body function. Care is directed to hypocalcemia. Rarely occurs

50. Hypomagnesemia (<1.4mEq/L) Contributing factors: – Malnutrition – Starvation – Diuretics – Aminoglcoside antibiotics – Hyperglycemia – Insulin administration

51. Hypomagnesemia (<1.4mEq/L) Assessment findings: *Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign. Hyperreflexia. Seizures *CV – ECG changes. Dysrhythmias. HTN *Resp. – Shallow resp. *GI – Dec. motility. Anorexia. Nausea

52. Hypomagnesemia (<1.4mEq/L) Interventions: – Eliminate contributing drugs – IV MgSO4 – Assess DTR’s hourly with MgSO4 – Diet Therapy

53. Hypermagnesemia (>2.0mEq/L) Contributing factors: – Increased Mg + intake – Decreased renal excretion

54. Hypermagnesemia (>2.0mEq/L) Assessment findings: Neuro – Reduced or weak DTR’s. Weak voluntary muscle contractions. Drowsy to the point of lethargy CV – Bradycardia, peripheral vasodilatation, hypotension. ECG changes.

55. Hypermagnesemia (>2.0mg/dL) Interventions – Eliminate contributing drugs – Administer diuretic – Calcium gluconate reverses cardiac effects – Diet restrictions

56. Acid- Base Balance – Acid: is a hydrogen (H+) donor. – Base: is an H+ acceptor (bind to hydrogen ions). – The pH is a measure of acid-base balance (hydrogen ion concentration in the blood). The more hydrogen ions, the more acidic is the medium and 7.4. Normal pH for humans is approximately 7.4. Normal values of acid-base balance components: ♦ PH: 7.35 - 7.45 ♦ PaC02: Normal = 35 to 45 mmHg ♦ HC03: Normal =22 to 26mEq/L ♦ PaO2: 80-100.

57. Types of Acid Base Imbalances Metabolic Acidosis Metabolic Alkalosis Respiratory acidosis Respiratory alkalosis

58. Types of Acid – base imbalance Metabolic Acidosis: Definition: Excessive absorption or retention of acid or excessive excretion of HC03. Cause: Ketoacidosis (DM) and prolonged fasting. renal disease Abnormal HCO3 losses( surgery, drains, or severe diarrhea.) Clinical manifestations: Headache, drowsiness, confusion, and weakness. Increased respiratory rate and depth hypotension, cold and sweaty skin pH below 7.35 and HCO3 below 22 mEq/L

59. Nursing management : 1. Monitor ABG value, 2. Administer sodium bicarbonate. 3. Monitor cardiovascular status closely, noting blood pressure, pulse rate and rhythm, capillary refill, and warmth and color of extremities.

60. Metabolic alkalosis Definition : Excessive loss of acid or excessive gain of HCO3 Causes: 1. prolonged vomiting or gastric suctioning. 2. Excessive intake of alkali e.g. antacids. 3. Respiratory insufficiency. 4. Massive blood transfusion

61. Clinical manifestations: – Tingling of the fingers and toes and tetany. – Slow, shallow respirations; possibly apnea. – Cardiac arrhythmias and death. – ABG studies: pH > 7.45 and HCO3 above 26 mEq/L Nursing management: 1. Monitor ABG values, 2. I&O, and for cardiac arrhythmias. 3. Correct electrolyte deficits, especially of potassium and sodium. 4. Monitor respiratory rate and pattern and auscultate lung sounds.

62. Respiratory acidosis: Increased arterial PaCo2 and decreased blood pH. Causes: 1. Chronic obstructive respiratory disorders, such as bronchial asthma 2. Acute disorders such as chest wall trauma, pulmonary edema, pneumothorax, pneumonia Clinical manifestations: 1. Increased pulse, BP, and respiratory rate 2. Mental cloudiness, and headache 3. ABG studies: pH below 7.35 and PaCo2 above 45 mmHg.

63. Nursing management 1. Monitor ABG, respiratory & cardiovascular status, & LOC. 2. Improve ventilation with 1. bronchodilators; 2. postural drainage; 3. antibiotic therapy; 4. regular coughing, 5. positioning, 6. turning, 7. deep breathing. 3. Maintain a quiet, relaxed environment & provide periods of complete rest. 4. Maintain fluid and electrolyte balance.

64. Respiratory Alkalosis decreased arterial Pco2 and increased blood pH. Causes: 1. Hyperventilation (most common) due to anxiety, hypoxia, improper mechanical ventilation 2. Fever

65. Clinical manifestations: 1. Light headache, deep rapid breathing, 2. Muscle twitching, convulsions, and cardiac dysarrhythmias. 3. ABG: pH above 7.45 and Pco2 below 35 mmHg. Nursing management 1. Monitor ABG values and respiratory status. 2. Treat the cause, e.g. ↓ pain, fever, and anxiety. 3. Encourage slow, deep breathing; instruct the client to breathe into air of a paper bag, if necessary, to reverse hyperventilation.

66. Thank you