FCC fluids and Electrolytes from Shenell D.

1. FLUIDS AND ELECTROLYTES

4. VARIATIONS IN FLUID CONTENT BODY FAT Because fat cells contain little water and lean tissue is rich in water, the more obese the person, the smaller the percentage of total body water compared with body weight. This is also true between sexes because females tend to have proportionally more body fat than males. There is also an increase in fat cells in older people

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

8. AVENUES BY WHICH WATER ENTERS AND LEAVES THE BODY

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

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

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

14. 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

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

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

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

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

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

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

37. CAUSES AND EFFECTS OF HYPOCALCEMIA Decreased Ionized Ca Large tranfusion with citrated blood Excess Loss Kidney Disease Draining fistula Decrease in GI Tract and Bone Absorption ↑ Magnesium ↑ Calcitonin ↓ Vitamin D ↓ Parathyroid Hormone HYPOCALCEMIA Bones Osteoporosis leading to Fractures CNS Tingling ↓ convulsions Other Abnormal deposits of calcium in body tissues Muscles Muscle spasm ↓ Tetany Cardiovascular System Dysrhythmias ↓ Cardiac arrest Inadequate Intake Dietary Deficit

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

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

42. HYPERCALCEMIA: Serum concentration > 10mg/dL Causes 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 Kidneys Stones ↓ Kidney Damage CNS ↓Deep-tendon reflexes ↓ Lethargy ↓ Coma Bones Bone pain ↓ Osteoporosis ↓ Fractures Muscles Muscle fatigue, hypotonia ↓ ↓ GI motility CV System Depressed activity ↓ Dysrhythmias ↓ Cardiac Arrest

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

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

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

49. 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

50. 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 High Serum Calcium Excretion of Magnesium By the GI tract

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

52. CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA CONFUSION DEPRESSION CRAMPS TETANY CONVULSIONS

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

57. NURSING MANAGEMENT OF PATIENT WITH FLUID AND ELECTROLYTE IMBALANCES

58. A 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, postural areas, pallor, bounding pulse, hypotension increased blood pressure 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

59. Pitting edema Dependent edema Refractory Edema

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

61. D Determined from analysis of patient data Diagnostic Title Possible 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

62. P EXPECTED PATIENT OUTCOMES 1,2. 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

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

73. NORMAL ACID-BASE BALANCE 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 Partial pressure of CO2 in the arterial blood: PCO2<35 mmHg = respiratory alkalosis PCO2>45 mmHg = respiratory acidosis 21-30 mmHg PaCO2 Identifies whether there is acidemia or alkalemia: pH<7.35 = acidosis; pH>7.45 = alkalosis 7.35-7.45 pH 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 Definition and Implications Normal Value Parameter

75. 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

77. INTERPRETING ARTERIAL BLOOD GASES RESULTS Look at the unrelated value. Decide whether or not compensation is happening 22-26 21-30 7.35-7.45 NORMAL Decide as to what may be the direct cause of the change in pH. pCO2 or HCO3? If PCO2, it’s respiratory, if HCO3, it’s metabolic Look at the HCO3 level. Is it normal or abnormal? Look at the pCO2. Is it normal or abnormal? Is the pH acidic or alkaline? ALKALOSIS ACIDOSIS CONDITION

78. 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

82. 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

83. 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

84. 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

85. 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

89. 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

90. 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

94. 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

95. 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

99. 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

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