Fluid and Electrolyte Imbalance

This is topic very helpful for understanding fluid therapy and electrolyte balance maintained in human body.

1. Fluid and electrolyte imbalance MR.JAGDISH SAMBAD Assistant Professor Balaji College of Nursing

2. FLUID AND ELECTROLYTE Fluid and electrolyte balance is a dynamic process that is crucial for life. Potential and actual disorders of fluid and electrolyte balance occur in every setting, with every disorder, and with a variety of changes that affect well people (e.g., increased fluid and sodium loss with strenuous exercise and high environmental temperature; inadequate intake of fluid and electrolytes) as well as those who are ill.

3. Electrolytes Electrolytes in body fluids are active chemicals which are The major cations (carry positive charges) - sodium , potassium, calcium, magnesium, and hydrogen ions. The major anions( carry negative charges ) -chloride , bicarbonate, phosphate, sulfate, and proteinate ions.

4. AMOUNT AND COMPOSITION OF BODY FLUIDS

5. REGULATION OF BODY FLUID COMPARTMENTS Osmosis and Osmolality fluid shifts through the membrane from the region of low solute concentration to the region of high solute concentration until the solutions are of equal concentration Tonicity is the ability of all the solutes to cause an osmotic driving force that promotes water movement from one compartment to another. Osmotic pressure is the amount of hydrostatic pressure needed to stop the flow of water by osmosis. It is primarily determined by the concentration of solutes. Oncotic pressure is the osmotic pressure exerted by proteins (e.g., albumin). Osmotic diuresis occurs when the urine output increases due to the excretion of substances such as glucose, mannitol , or contrast agents in the urine.

6. Diffusion is the natural tendency of a substance to move from an area of higher concentration to one of lower concentration. It occurs through the random movement of ions and molecules. Filtration Movement of water and solutes occurs from an area of high hydrostatic pressure to an area of low hydrostatic pressure. Filtration allows the kidneys to filter 180 L of plasma per day.

7. Sodium–Potassium Pump The sodium concentration is greater in the ECF than in the ICF, and because of this, sodium tends to enter the cell by diffusion. This tendency is offset by the sodium–potassium pump, which is located in the cell membrane and actively moves sodium from the cell into the ECF. Conversely, the high intracellular potassium concentration is maintained by pumping potassium into the cell. By definition, active transport implies that energy must be expended for the movement to occur against a concentration gradient.

8. Fluid imbalances

9. FLUID VOLUME DEFICIT (HYPOVOLEMIA) Fluid volume deficit (FVD) occurs when loss of extracellular fluid volume exceeds the intake of fluid

10. Causes: FVD results from loss of body fluids and occurs more rapidly when coupled with decreased fluid intake . It includes abnormal fluid losses, such as those resulting from vomiting, diarrhea, GI suctioning, and sweating, and decreased intake, as in nausea or inability to gain access to fluids . Additional risk factors include diabetes insipidus, adrenal insufficiency, osmotic diuresis, hemorrhage, and coma.

11. Clinical Manifestations acute weight loss decreased skin turgor oliguria concentrated urine postural hypotension a weak, rapid heart rate flattened neck veins increased temperature decreased central venous pressure cool, clammy skin related to peripheral vasoconstriction thirst anorexia muscle weakness cramps

12. Physiology/Pathophysiology Hematocrit level is greater than normal because the red blood cells become suspended in a decreased plasma volume. Serum electrolyte changes may also exist. Hypokalemia occurs with GI and renal losses. Hyperkalemia occurs with adrenal insufficiency. Hyponatremia occurs with increased thirst and ADH release. Hypernatremia results from increased insensible losses and diabetes insipidus. Urine specific gravity is increased in relation to the kidneys’ attempt to conserve water and decreased with diabetes insipidus. Urine osmolality is greater than 450 mOsm /Kg, since the kidneys try to compensate by conserving water.

13. Medical Management When the deficit is not severe, the oral route is preferred, provided the patient can drink. When fluid losses are acute or severe, however, the IV route is required . Isotonic electrolyte solutions (e.g., lactated Ringer’s or 0.9% sodium chloride) are frequently used. As soon as the patient becomes normotensive , a hypotonic electrolyte solution (e.g., 0.45% sodium chloride) is often used to provide both electrolytes and water for renal excretion of metabolic wastes. Accurate and frequent assessments of intake and output, weight, vital signs, central venous pressure, level of consciousness, breathe sounds, and skin color should be performed to determine when therapy should be slowed to avoid volume overload.

14. Nursing Management To assess for FVD, the nurse monitors and measures fluid intake and output at least every 8 hours and sometimes hourly. Skin and tongue turgor is monitored on a regular basis. The degree of oral mucous membrane moisture is also assessed; a dry mouth may indicate either FVD or mouth breathing. Urinary concentration is monitored by measuring the urine specific gravity. In a volume-depleted patient, the urinary specific gravity should be above 1.020, indicating healthy renal conservation of fluid. Mental function is eventually affected in severe FVD as a result of decreasing cerebral perfusion. Decreased peripheral perfusion can result in cold extremities .

15. PREVENTING FVD To prevent FVD, the nurse identifies patients at risk and takes measures to minimize fluid losses. For example, if the patient has diarrhea, diarrhea control measures should be implemented and replacement fluids administered. These measures may include administering antidiarrheal medications and small volumes of oral fluids at frequent intervals.

16. FLUID VOLUME EXCESS (HYPERVOLEMIA ) Fluid volume excess (FVE) refers to an isotonic expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF. It is always secondary to an increase in the total body sodium content, which, in turn, leads to an increase in total body water.

17. Cause FVE may be related to simple fluid overload or diminished function of the homeostatic mechanisms responsible for regulating fluid balance. Contributing factors can include heart failure, renal failure, and cirrhosis of the liver . Another contributing factor is consumption of excessive amounts of table or other sodium salts.

18. Signs and symptoms edema, distended neck veins, and crackles (abnormal lung sounds). Other manifestations include tachycardia; increased blood pressure, pulse pressure, and central venous pressure ; increased weight ; increased urine output; and shortness of breath and wheezing.

19. Assessment and Diagnostic Findings BUN Hematocrit levels. Chest X-ray Serum sodium levels.

20. Medical Management PHARMACOLOGIC THERAPY Diuretics HEMODIALYSIS NUTRITIONAL THERAPY dietary restriction of sodium and fluid. Lemon juice, onions, and garlic are excellent substitute flavorings, although some patients prefer salt substitutes. Patients may need to use distilled water when the local water supply is very high in sodium.

21. Electrolytes imbalances

22. SODIUM DEFICIT (HYPONATREMIA)

23. Causes Vomiting Diarrhea Fistulas Sweating Dilutional Hyponatremia In water intoxication ( dilutional hyponatremia ), the patient’s serum sodium level is diluted by an increase in the ratio of water to sodium. This causes water to move into the cell, so that the patient develops an ECF volume excess. SIADH

24. Clinical manifestations Poor skin turgor, dry mucosa, decreased saliva production , orthostatic fall in blood pressure, nausea , and abdominal cramping altered mental status anorexia , muscle cramps , feeling of exhaustion. When the serum sodium level drops below 115 mEq /L (115 mmol /L), signs of increasing intracranial pressure, such as lethargy, confusion, muscle twitching, focal weakness, hemiparesis, papilledema, and seizures, may occur

25. Medical Management SODIUM REPLACEMENT Careful administration of sodium In SIADH, the administration of hypertonic saline solution alone cannot change the plasma sodium concentration. Excess sodium would be excreted rapidly in highly concentrated urine. With the addition of the diuretic furosemide (Lasix), urine is not concentrated and isotonic urine is excreted to effect a change in water balance . In patients with SIADH, in whom water restriction is difficult, lithium or demeclocycline can antagonize the osmotic effect of ADH on the medullary collecting tubule.

26. SODIUM EXCESS (HYPERNATREMIA ) Hypernatremia is a higher-than-normal serum sodium level (exceeding 145 mEq /L [145 mmol /L ]). causes Hyperaldosteronism Renal failure Corticosteroids Increase in oral Na intake Na containing IV fluids Decreased urine output with increased urine concentration Fluid deprivation

27. Clinical manifestations thirst . dry , swollen tongue and sticky mucous membranes . Flushed skin, peripheral and pulmonary edema , postural hypotension , and increased muscle tone and deep tendon reflexes restlessness and weakness in moderate hypernatremia disorientation, delusions, and hallucinations in severe hypernatremia .

28. Medical Management a gradual lowering of the serum sodium level by the infusion of a hypotonic electrolyte solution (e.g., 0.3% sodium chloride) or an isotonic no saline solution (e.g., dextrose 5% in water [D5W]).

29. POTASSIUM DEFICIT (HYPOKALEMIA) Hypokalemia (below-normal serum potassium concentration) usually indicates an actual deficit in total potassium stores, fallen below 3 mEq /L (3 mmol /L). Pathophysiology – Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive to normal stimuli

30. Contributing factors: Diuretics Shift into cells Digitalis Water intoxication Corticosteroids Diarrhea Vomiting

31. Clinical manifestations

32. Assessment and Diagnostic Findings In hypokalemia, the serum potassium concentration is less than the lower limit of normal. Electrocardiographic (ECG) changes can include flat T waves and/or inverted T waves, suggesting ischemia, and depressed ST segments. An elevated U wave is specific to hypokalemia.

33. Management Assess and identify those at risk Encourage potassium-rich foods K+ replacement (IV or PO) Monitor lab values D/c potassium-wasting diuretics Treat underlying cause

34. Nursing Management Fatigue , anorexia, muscle weakness, decreased bowel motility, paresthesias , and dysrhythmias are signals that warrant assessing the serum potassium concentration. Careful watch for signs.

35. POTASSIUM EXCESS (HYPERKALEMIA) Hyperkalemia (greater-than-normal serum potassium concentration) i.e. above 6mEq/L. Pathophysiology – An Inc. in K+ causes increased excitability of cells

36. Causes Increase in K+ intake Renal failure K + sparing diuretics Shift of K+ out of the cells

37. Clinical manifestations

38. often occurring at a serum potassium level greater than 6 mEq /L (6 mmol /L), are peaked, narrow T waves; ST-segment depression; and a shortened QT interval. If the serum potassium level continues to rise, the PR interval becomes prolonged and is followed by disappearance of the P waves. Finally, there is decomposition and prolongation of the QRS complex.

39. Medical Management Need to restore normal K+ balance: Eliminate K+ administration either orally or by retention enema Inc. K+ excretion Lasix Kayexalate (Polystyrene sulfonate ) Infuse glucose and insulin Cardiac Monitoring

40. Nursing Management The nurse observes for signs of muscle weakness and dysrhythmias. The presence of paresthesias is noted, as are GI symptoms such as nausea and intestinal colic.

41. CALCIUM DEFICIT (HYPOCALCEMIA) Hypocalcemia (lower-than-normal serum concentration of calcium) occurs in a variety of clinical situations. Contributing factors : Dec. oral intake Lactose intolerance Dec. Vitamin D intake End stage renal disease Diarrhea Acute pancreatitis Hypophosphatemia Immobility Removal or destruction of parathyroid gland

42. Clinical manifestations Neuro –Irritable muscle twitches . Tetany . Positive Trousseau’s sign. Positive Chvostek’s sign. Resp. – Resp. failure d/t muscle tetany . CV – Dec. HR., Dec. BP, diminished peripheral pulses GI – Inc. motility. Inc. BS. Diarrhea

43. Trousseau’s sign can be elicited by inflating a blood pressure cuff on the upper arm to about 20 mm Hg above systolic pressure; within 2 to 5 minutes, carpopedal spasm (an adducted thumb, flexed wrist and metacarpophalangeal joints, extended interphalangeal joints with fingers together) will occur as ischemia of the ulnar nerve develops

44. Chvostek’s sign consists of twitching of muscles supplied by the facial nerve when the nerve is tapped about 2 cm anterior to the earlobe, just below the zygomatic arch.

45. Medical Management Drug Therapy Calcium supplements Vitamin D Diet Therapy High calcium diet Prevention of Injury Seizure precautions

46. Nursing Management Seizure precautions are initiated when hypocalcaemia is severe. The status of the airway is closely monitored because laryngeal stridor can occur. Safety precautions are taken, as indicated, if confusion is present. People at high risk for osteoporosis are instructed about the need for adequate dietary calcium intake; if not consumed in the diet, calcium supplements should be considered.

47. CALCIUM EXCESS (HYPERCALCEMIA ) Hypercalcemia (excess of calcium in the plasma) is a dangerous imbalance when severe; in fact, hypercalcemic crisis has a mortality rate as high as 50% if not treated promptly. The serum calcium level is greater than 10.5 mg/ dL (2.6 mmol /L). Causes Excessive calcium intake Excessive vitamin D intake Renal failure Hyperparathyroidism Malignancy Hyperthyroidism

48. Clinical manifestations 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

49. Assessment and Diagnostic Findings ECG - Cardiovascular changes may include a variety of dysrhythmias and shortening of the QT interval and ST segment. The PR interval is sometimes prolonged. X-rays may reveal the presence of osteoporosis, bone cavitation, or urinary calculi. The Sulkowitch urine test analyzes the amount of calcium in the urine; in hypercalcemia , dense precipitation is observed due to hypercalciuria .

50. Medical management Eliminate calcium administration Drug Therapy Isotonic NaCL (Inc. the excretion of Ca) Diuretics Calcium reabsorption inhibitors (Phosphorus) Cardiac Monitoring

51. Nursing management Increase patient mobility encourage fluids When encouraging oral fluids, the nurse considers the patient’s likes and dislikes. Fluids containing sodium should be administered unless contraindicated by other conditions encouraged to drink 3 to 4 quarts of fluid daily. Adequate fiber should be provided in the diet to offset the tendency for constipation. Safety precautions are taken, as necessary, when mental symptoms of hypercalcemia are present.

52. MAGNESIUM DEFICIT (HYPOMAGNESEMIA ) below-normal serum magnesium concentration. The normal serum magnesium level - 1.5 to 2.5 mEq /L (or 1.8–3.0 mg/ dL ; 0.8–1.2 mmol /L). Contributing factors: Malnutrition Starvation Diuretics Aminoglycoside antibiotics Hyperglycemia Insulin administration

53. Clinical manifestations Neuro - Positive Trousseau’s sign. Positive Chvostek’s sign. Hyperreflexia . Seizures , athetoid movements (slow, involuntary twisting and writhing). CV – ECG changes. Dysrhythmias. HTN Resp . – Shallow resp. GI – Dec. motility. Anorexia. Nausea

54. Medical management Eliminate contributing drugs IV MgSO4 Assess DTR’s hourly with MgSO4 Diet Therapy

55. Nursing management Diet therapy- magnesium rich foods Teach to stop contributing drugs- diuretic or laxative Provide help for avoidance of alcohol consumption.

56. MAGNESIUM EXCESS (HYPERMAGNESEMIA) Hypermagnesemia is a greater-than-normal serum concentration of magnesium. The serum magnesium level is greater than 2.5 mEq /L or 3.0 mg/ dL (1.25 mmol /L). Contributing factors: Increased Mg intake Decreased renal excretion

57. Clinical Manifestations Neuro – Reduced or weak DTR’s. Weak voluntary muscle contractions. Drowsy to the point of lethargy CV – Bradycardia, peripheral vasodilatation, hypotension. ECG changes- a prolonged PR interval, tall T waves, and a widened QRS.

58. management Eliminate contributing drugs Administer diuretic Calcium gluconate reverses cardiac effects Diet restrictions

59. Nursing management Careful observation Check vital signs Check DTR

60. PHOSPHORUS DEFICIT (HYPOPHOSPHATEMIA) Hypophosphatemia is a below-normal serum concentration of inorganic phosphorus. The serum phosphorus level is less than 2.5 mg/ dL (0.80 mmol /L) in adults . Contributing Factors: Malnutrition Starvation Hypercalcemia Renal failure Uncontrolled DM

61. Clinical manifestations Neuro – Irritability, confusion CV – Dec. contractility Resp . – Shallow respirations Musculoskeletal - Rhabdomyolysis Hematologic – Inc. bleeding Dec. platelet aggregation

62. management Treat underlying cause Oral replacement with vit . D IV phosphorus (Severe) Diet therapy Foods high in oral phosphate

63. Nursing management Careful observation and monitoring Food rich in phosphate.

64. PHOSPHORUS EXCESS (HYPERPHOSPHATEMIA) Hyperphosphatemia is a serum phosphorus level that exceeds normal. The serum phosphorus level exceeds 4.5 mg/ dL (1.5 mmol /L) in adults. Rarely occurs.

65. Clinical Manifestations Tetany Anorexia , nausea, vomiting, muscle weakness, hyperreflexia , and tachycardia may occur. Decreasing urine output, impairing vision, and producing palpitations.

66. Medical management Avoid Vitamin D supplements Restriction of dietary phosphate. Give calcium binding antacids, phosphate binding gels or antacids. Dialysis.

67. Nursing Management Low phosphorus diet Teach to avoid phosphate binding substances such as laxatives and enemas.

68. CHLORIDE DEFICIT (HYPOCHLOREMIA) The normal serum chloride level is 96 to 106 mEq /L (96–106 mmol /L) As chloride decreases (usually because of volume depletion), sodium and bicarbonate ions are retained by the kidney to balance the loss. Bicarbonate accumulates in the ECF, which raises the pH and leads to hypochloremic metabolic alkalosis.

69. Clinical Manifestations Metabolic alkalosis Hyper-excitability of muscles, tetany , and hyperactive deep tendon reflexes, weakness, twitching, and muscle cramps may result. seizures and coma.

70. Medical Management correcting the cause of hypochloremia and contributing electrolyte and acid–base imbalances. Normal saline (0.9% sodium chloride) or half-strength saline (0.45% sodium chloride) solution is administered IV to replace the chloride. Foods high in chloride are provided; these include tomato juice, salty broth, canned vegetables, processed meats, and fruits. Ammonium chloride, an acidifying agent, may be prescribed to treat metabolic alkalosis; the dosage depends on the patient’s weight and serum chloride level.

71. Nursing Management The nurse monitors intake and output, arterial blood gas values, and serum electrolyte levels, Check patient’s level of consciousness and muscle strength and movement Vital signs are monitored and respiratory assessment is carried out frequently. The nurse teaches the patient about foods with high chloride content.

72. CHLORIDE EXCESS (HYPERCHLOREMIA) Hyperchloremia exists when the serum level exceeds 106 mEq /L (106 mmol /L).

73. Clinical Manifestations same as those of metabolic acidosis, hypervolemia, and hypernatremia. Tachypnea ; weakness ; lethargy ; deep , rapid respirations; diminished cognitive ability; hypertension occur.

74. Medical Management Lactated Ringer’s solution may be prescribed to convert lactate to bicarbonate in the liver, which will increase the base bicarbonate level and correct the acidosis. Sodium bicarbonate may be given IV to increase bicarbonate levels, which leads to the renal excretion of chloride ions as bicarbonate and chloride compete for combination with sodium. Diuretics may be administered to eliminate chloride as well. Sodium, fluids, and chloride are restricted.

75. Nursing Management Monitoring vital signs, arterial blood gas values, and intake and output is important to assess the patient’s status and the effectiveness of treatment . Assessment findings related to respiratory, neurologic, and cardiac systems are documented and changes discussed with the physician. The nurse teaches the patient about the diet that should be followed to manage hyperchloremia .

76. Acid base imbalances

77. Acid base disturbances Acute and chronic metabolic acidosis Acute and chronic metabolic alkalosis Acute and chronic respiratory acidosis Acute and chronic respiratory alkalosis

78. ACUTE AND CHRONIC METABOLIC ACIDOSIS (BASE BICARBONATE DEFICIT ) Metabolic acidosis is a clinical disturbance characterized by a low pH (increased Concentration) and a low plasma bicarbonate concentration. It can be produced by a gain of hydrogen ion or a loss of bicarbonate. Low pH (less than 7.35 ).   Clinical Manifestations Headache, confusion, drowsiness, increased respiratory rate and depth, nausea, and vomiting. Peripheral vasodilation and decreased cardiac output occur when the pH falls below 7. Additional physical assessment findings include decreased blood pressure, cold and clammy skin, dysrhythmias, and shock.

79. Assessment and Diagnostic Findings Arterial blood gas measurements. Expected blood gas changes include a low bicarbonate level (less than 22 mEq /L ) and a low pH (less than 7.35). ECG will detect dysrhythmias caused by the increased potassium . Medical Management When necessary, bicarbonate is administered if the pH is less than 7.1 and the bicarbonate level is less than 10. Alkalizing agents may be given if the serum bicarbonate level is less than 12 mEq /L. Treatment modalities may also include hemodialysis or peritoneal dialysis.

80. ACUTE AND CHRONIC METABOLIC ALKALOSIS (BASE BICARBONATE EXCESS ) Metabolic alkalosis is a clinical disturbance characterized by a high pH (decreased H+ concentration) and a high plasma bicarbonate concentration. It can be produced by a gain of bicarbonate or a loss of H+. A pH greater than 7.45 Clinical Manifestations Alkalosis is primarily manifested by symptoms related to decreased calcium ionization, such as tingling of the fingers and toes, dizziness, and hypertonic muscles. The ionized fraction of serum calcium decreases in alkalosis as more calcium combines with serum proteins.

81. Assessment and Diagnostic Findings Evaluation of arterial blood. The urine chloride concentration should be less than 15 mEq /L when decreased chloride levels and hypovolemia occur. Medical Management Sufficient chloride must be supplied for the kidney to absorb sodium with chloride (allowing the excretion of excess bicarbonate). In patients with hypokalemia, potassium is administered as KCl to replace both K+ and Cl−losses. Histamine-2 receptor antagonists, such as cimetidine (Tagamet), reduce the production of gastric HCl . Carbonic anhydrase inhibitors are useful in treating metabolic alkalosis in patients who cannot tolerate rapid volume expansion (e.g., patients with heart failure).

82. ACUTE AND CHRONIC RESPIRATORY ACIDOSIS (CARBONIC ACID EXCESS ) Respiratory acidosis is a clinical disorder in which the pH is less than 7.35 and the PaCO2 is greater than 42 mm Hg. It may be either acute or chronic. Clinical Manifestations Increased pulse and respiratory rate, increased blood pressure, mental cloudiness, and feeling of fullness in the head. Intracranial pressure may increase, resulting in papilledema and dilated conjunctival blood vessels.  

83. Assessment and Diagnostic Findings Arterial blood gas evaluation reveals a pH less than 7.35, a PaCO2 greater than 42 mm Hg Serum electrolyte levels Chest x-ray for determining any respiratory disease ECG to identify any cardiac involvement as a result of chronic obstructive pulmonary disease Medical Management Treatment is directed at improving ventilation Pharmacologic agents are used as indicated. For example, bronchodilators help reduce bronchial spasm, antibiotics are used for respiratory infections, and thrombolytic or anticoagulants are used for pulmonary emboli.

84. ACUTE AND CHRONIC RESPIRATORY ALKALOSIS (CARBONIC ACID DEFICIT ) Respiratory alkalosis is a clinical condition in which the arterial pH is greater than 7.45 and the PaCO2 is less than 38 mm Hg. As with respiratory acidosis, acute and chronic conditions can occur. Respiratory alkalosis is always due to hyperventilation, which causes excessive “blowing off” of CO2 and, hence, a decrease in the plasma carbonic acid concentration. Clinical Manifestations Clinical signs consist of lightheadedness due to vasoconstriction and decreased cerebral blood flow, inability to concentrate, numbness and tingling from decreased calcium ionization, tinnitus, and at times loss of consciousness. Cardiac effects of respiratory alkalosis include tachycardia and ventricular and atrial dysrhythmias.

85. Assessment and Diagnostic Findings Analysis of arterial blood gases Evaluation of serum electrolytes is indicated to identify any decrease in potassium as hydrogen is pulled out of the cells in exchange for potassium; decreased calcium Medical Management If the cause is anxiety, the patient is instructed to breathe more slowly to allow CO2 to accumulate or to breathe into a closed system (such as a paper bag). A sedative may be required to relieve hyperventilation in very anxious patients.

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