AY24-25 Fall-NUR-2332-Adult Health Nursing-Week 4-Fluid Volume Disturbances & Electrolyte Imbalances-Part 2 PDF

College of Health Sciences Department of Nursing Bachelor of Science in Nursing (BSN) Program NUR- 3343 Adult Health Nursing Presented by: Dr. Mona Afifi  Week 4: Fluid Volume Disturbances and Electrolyte Imbalances...

College of Health Sciences Department of Nursing Bachelor of Science in Nursing (BSN) Program NUR- 3343 Adult Health Nursing Presented by: Dr. Mona Afifi  Week 4: Fluid Volume Disturbances and Electrolyte Imbalances Student Leaning Outcomes (SLOs) PLO1: Demonstrate a sound knowledge of the essential concepts and theories related to the nursing practice. By the end of this session students will be able to: 1. Identify causes of Hypo-hypernatremia, Hypo-hyperkalemia, Hypo- hypercalcemia, Hypo-hypermagnesemia, Hypo-hyperphosphatemia. (CLO1) 2. Distinguish clinical manifestations in each electrolyte imbalance. (CLO2) 3. Differentiate medical management and nursing interventions in each electrolyte imbalance. (CLO4)  Lecture Outline ✔ Introduction ✔ Hyponatremia and Hypernatremia ✔ Hypokalemia and Hyperkalemia ✔ Hypocalcemia and Hypercalcemia ✔ Hypomagnesemia and Hypermagnesemia ✔ Hypophosphatemia and Hypermagnesemia ✔ Critical Thinking Question https://youtu.be/nSH8qce-epw?si=mDjiQyE_5LoaunZP https://youtu.be/-PaHC8fleO0?si=etS0YLyRimZetVIn  Introduction  Sodium ✔ Plasma sodium concentration represents the ratio of total body sodium to total body water. ✔ Determinant of the osmolality of the ECF* ✔ Regulator of ECF* volume. ✔ Sodium imbalance is common in clinical practice. Normal Serum Sodium is 135 to 145 mEq/L *ECF : Extracellular Fluid  Introduction Sodium is regulated by ADH, thirst, and the renin– angiotensin–aldosterone system. A loss or gain of sodium is usually accompanied by a loss or gain of water. Sodium also functions in establishing the electrochemical state necessary for muscle contraction and the transmission of nerve impulse  Hyponatremia  Refers to a serum sodium level.  primarily occurs due to an imbalance of water rather than Serum Sodium < 135 mEq sodium.  Below normal level (less than 135 mEq/L).  Causes: 1. Increased sodium excretion ✔ Vomiting ✔ Sweating ✔ Diarrhea ✔ Diuretics ✔ Fistulas ✔ Adrenal insufficiency 2. Inadequate sodium intake ✔ Fasting ✔ Low sodium diet As the extracellular sodium level decreases, the cellular fluid becomes relatively more concentrated and pulls water into the cells  Hyponatremia (Continued) Predisposing Conditions: 3. Dilution of serum sodium  Syndrome of Inappropriate (Dilutional Hyponatremia) Antidiuretic Hormone (SIADH)  In water intoxication Excessive ADH activity Sodium level is diluted by: an increase in the ratio  Hyperglycemia of water to sodium  Use of tap-water enemas This causes water to move into the cell  Irrigation of gastric tubes with water instead of normal saline  Hyponatremia (Continued)  Clinical Manifestations  Labs indicates ✔ ↓ Serum Sodium ✔ ↓ Urine Sodium ✔ ↓ Urine Specific Gravity ✔ ↓ Urine Osmolality  Hyponatremia (Continued) Remember..!!! If Mild hyponatremia is caused by water excess, Fluid Restriction Loop Diuretics may be the only treatment may be given. If severe hyponatremia, Small amount (100-150 Ml/IV) of IV hypertonic saline (e.g., 3% saline)  Hyponatremia (Continued)  Nursing Interventions Monitors fluid intake and output, and weights. Focus assessment of the level of consciousness and neuromuscular response. Provide safety and seizure precautions. Encourage foods and fluids high in sodium. Hyponatremia precipitates lithium toxicity in patients taking lithium Lithium is used to treat mania that is part of bipolar disorder (manic-depressive illness)  Hypernatremia  Sodium level (exceeding 145 mEq/L) Let’s compare…!  Urine Specific Gravity  Causes: 1. Decreased sodium excretion  Corticosteroids  Cushing’s syndrome ( aldosterone) 2. Increased water loss  Diabetes Insipidus  Watery diarrhea 3. Increased sodium intake 4. administration of hypertonic enteral feedings without adequate water supplements  Hypernatremia  Results in a relatively concentrated ECF  Causing the water to be pulled from the cells into the ECF, resulting in cellular dehydration and a more concentrated ECF The clinical manifestations of hypernatremia are primarily neurologic due to increased plasma osmolality caused by increased plasma sodium concentration.  Hypernatremia (Continued)  Clinical Manifestations Primary characteristics is “Thirst” a dry, swollen tongue and sticky mucous membranes; flushed skin For moderate hypernatremia  Restlessness and weakness For severe hypernatremia  Disorientation  Delusion and hallucinations  Brain damage  increased muscle tone and deep tendon reflexes (DTRs)  Hypernatremia (Continued)  Management  Gradual lowering of serum sodium level  Using hypotonic solution ( most preferable) (e.g. 0.3% Sodium Chloride) it allows a gradual reduction in the serum sodium level or  Isotonic nonsaline solution (e.g. D5W)  Diuretics may also be prescribed to treat sodium gain.  Hypernatremia (Continued)  Nursing Interventions ✔ Assess for losses of water; low water intake. ✔ Monitor I & O and Weigh daily ✔ Avoidance of foods high in sodium ✔ Offering fluids at regular intervals ✔ For Diabetes Insipidus (adequate water intake) ✔ Provide frequent oral care  Potassium  Potassium is the major intracellular electrolyte  98% of the body’s potassium is inside the cells.  The remaining 2% is in the ECF and is important in neuromuscular function.  Potassium influences both skeletal and cardiac muscle activity.  Alterations in Potassium concentration change myocardial irritability and rhythm.  80% of the potassium excreted daily by way of the kidneys;  20% of “K” is lost through the bowel and in sweat.  Hypokalemia  Potassium level (< 3.5 mEq/L)  Causes Normal Potassium is 3.5 to 5.0 mEq/L 1. Actual total body potassium loss ✔ Corticosteroid 3. Inadequate potassium intake ✔ Diuretics ✔ Fasting ✔ Cushing’s syndrome ✔ Vomiting, Diarrhea 4. Dilution of serum potassium 2. Movement of potassium from the ECF to ICF ✔ Water intoxication ✔ Alkalosis Acid-base balance affects serum potassium, a rise in the serum pH (decrease in H+ concentration) will result in a shift of H+ out of the cell and potassium into the cell. The reverse occurs during acidemia with a shift of potassium out of the cell. ✔ Hyperinsulinism 5. Magnesium deficiency  Hypokalemia (Continued)  Clinical Manifestations Normal ECG  Hypokalemia (Continued)  Management If conventional measures is not effective  For mild and moderate hypokalemia Precautions with IV Potassium Oral replacement therapy  Never given by IV push or  For severe hypokalemia  Never given by IM or Subcutaneous IV replacement therapy  Always diluted &  Administered using an infusion device  Hypokalemia (Continued) Nursing Interventions ✔ Monitor cardiovascular, respiratory & Place the patient on cardiac monitor.  Encourage intake of foods and fluids high in potassium Banana Peas Red meat Coffee Oranges Baked potatoes Salmon Cola Dried fruits Tomatoes Leafy vegetable Tea  Observe signs of metabolic alkalosis Hypoventilation Tetany Tachycardia Changes in mentation  Hypokalemia (Continued) Nursing Interventions ✔ Potassium should be administered only after adequate urine flow has been established. A decrease in urine volume (oliguria) to less than 20 mL/h for 2 consecutive hours is an indication to stop the potassium infusion. ✔ Oral potassium supplements can produce small bowel lesions; therefore, the patient must be assessed for abdominal distention, pain, or GI bleeding.  Hyperkalemia  Potassium Level (> 5.0 mEq/L)  More dangerous because: cardiac arrest is more  Causes: frequently associated with high 1. Decreased renal excretion of potassium  Kidney disease serum potassium levels.  Adrenal insufficiency (e.g., Addison’s disease)  because deficient adrenal hormones lead to sodium loss and potassium retention.  Potassium –retaining diuretics 2. Movement of potassium from the ICF to ECF  Tissue damage  Hyperuricemia  Acidosis: potassium moves out of the cells and into the ECF. This occurs as hydrogen ions enter the cells to buffer the pH of the ECF  Hyperkalemia (Continued)  Clinical Manifestations:  Hyperkalemia (Continued)  Management  Monitor ECG to detect changes  Administered potassium-excreting diuretics (if renal function is not impaired)  Kayexalate to treat high levels of potassium ( in patients with renal impairment  Hypertonic glucose and regular insulin To move excess potassium into the cells. Beta-2 agonist Administered IV Calcium if hyperkalemia is severe, move potassium into the cells to avert myocardial excitability. stabilize cardiac cell membranes. Dialysis (if hyperkalemia is severe ; critically high)  Hyperkalemia (Continued)  Nursing Interventions ✔ Identify risk or cause of hyperkalemia ✔ Monitor respiratory rate and depth ✔ Encourage coughing and deep breathing exercises ✔ Monitor heart rate and rhythm (be aware that cardiac arrest can occur)  Monitor urinary output  Assess LOC and neuromuscular functions  Hypocalcemia  Serum Calcium Level (< 9.0 mg/dL) Cause: Normal Calcium is 9.0 to 10.5 mg/dL -Primary or surgical hypoparathyroidism -Inflammation of pancreas, burns, peritonitis, malignancies -Excessive GI losses (diarrhea, Fat malabsorption syndromes, chronic laxative use) -Diuretic and terminal phase of renal failure -Inadequate dietary intake of Vit.D -Alcoholism  Hypocalcemia (Continued)  Clinical Manifestations Positive Trousseau’s sign and Chvostek’s sign Others include:  Hypotension  Twitches, Tetany , Seizures  Laryngeal Stridor  Dysphagia  Numbness, tingling around the mouth or in the extremities  Hypocalcemia (Continued)  Management ✔ Parenteral calcium salt (eg. calcium gluconate, calcium chloride) Calcium gluconate-not often use because more irritating -can also cause sloughing of tissue  Too rapid IV administration of calcium can cause cardiac arrest  Vit. D therapy to increase calcium absorption  Aluminum hydroxide, calcium acetate, calcium carbonate antacids -to decrease elevated phosphorus before treating hypocalcemia (for patient with chronic renal failure) Remember: High Ca intake inhibits P uptake from the gut, and a high P intake may decrease the absorption of Ca, both due to the formation of Ca-P salts.  Increase dietary intake of calcium 1,000-1,500 mg/day  Hypocalcemia (Continued) Nursing Interventions  Monitor heart rate and rhythm  Assess respiratory rate, rhythm, and effort  Observe for neuromuscular irritability, including tetany or seizure  Assess for Chvostek’s and Trousseau’s signs  Review client’s drug regimen such as use of insulin, digoxin.  Discuss the use of laxatives and antacids  Identify the sources of increase calcium and vit.D in diet (oily fish, meat, egg yolk)  Hypercalcemia Cause Serum calcium level -Hyperparathyroidism, hyperthyroidism, (>10.5 mg/dL) malignancies -Excessive or prolonged use of Vit.A & D, calcium Is a dangerous imbalance when containing antacids. severe; -Prolonged use of thiazide, diuretics, theophylline, hypercalcemic crisis has a lithium mortality rate as high as 50% if -Multiple fractures, bone tumors, osteoporosis not treated promptly. -Prolonged immobilization -Milk-alkali syndrome as side effect of prolonged Remember: as blood calcium levels milk and antacid self-medication for ulcer rise, phosphate levels fall. -hypophosphatasia, hyperproteinemia -Anticancer drugs: tamoxifen, androgens, estrogens  Hypercalcemia (Continued)  Clinical Manifestations Hypercalcemia reduces neuromuscular excitability  it suppresses activity at the myoneural junction so reduces the transmission of action potential from nerve to the muscle.  Common symptoms  Anorexia  Nausea  Vomiting  Constipation  Hypercalcemia (Continued)  Medical Management  IV administration of 0.9% sodium chloride  This temporarily dilutes calcium level  Increase urinary calcium excretion  Administering IV phosphate  Can cause a reciprocal drop in calcium serum  Furosemide (use in conjunction with saline)  This increase calcium excretion  Calcitonin  To lower serum calcium level  Reduces bone resorption  Increases deposit calcium and phosphorus in bones  Increases urinary excretion of calcium and phosphorus  Hypercalcemia (Continued)  Medical Management  Corticosteroid  To decrease bone turnover and tubular reabsorption (for patient with myelomas, lymphomas, leukemias)  Mithramycin (cytotoxic antibiotic)  Inhibits bone resorption and lowers serum calcium level  IV phosphate therapy  With extreme caution when use (because of severe calcification, hypotension, tetany and acute renal failure)  Calcium and phosphate are inversely related: as blood calcium levels rise, phosphate levels fall. This is because phosphate binds to calcium reducing the available free calcium within the bloodstream.  Hypercalcemia (Continued)  Nursing Interventions  Monitor cardiac rate and rhythm  Assess level of consciousness  Monitor intake and output  Encourage fluid intake of 3 to 4 L/day  Encourage frequent repositioning and ROM with caution  Provide safety measures, gentle handling when moving patient  Noting use of calcium-elevating drugs  Identify and restrict sources of calcium intake  Hypomagnesemia -refers to a below-normal serum Cause magnesium concentration  Biliary or intestinal fistula, surgery, laxative abuse, The normal serum magnesium diarrhea, impaired GI absorption, gastric or colon level is 1.5 to 2.5 mEq/L cancer.  Protein or calorie malnutrition, enteral or parenteral feeding without adequate magnesium replacement  Prolonged IV infusion of magnesium free solutions  Chronic alcoholism, pancreatitis  Renal losses, drugs that affect magnesium balance  Diabetic ketoacidosis, severe burns, hyperthyroidism  Hypomagnesemia (Continued)  Clinical Manifestations  Hypomagnesemia (Continued)  Management  Magnesium Sulfate (IM) or Magnesium Hydroxide (PO)  Magnesium-based antacids  Mylanta  Maalox  Gelusil  Riopan  Hypomagnesemia (Continued)  Nursing Interventions  Monitor for signs of digoxin intoxication  Watch out for:  nausea and vomiting  blurred vision  atrial dysrhythmias and heart blocks  Monitor status of airway and swallowing  Assess level of consciousness  Provide quite environment  Place footboard or cradle on bed  Hypomagnesemia (Continued)  Nursing Interventions  Auscultate bowel sounds  Encourage intake of dairy products, green leafy vegetables  Instruct proper use of laxatives and diuretics  Observe signs of magnesium toxicity during replacement therapy  Hypermagnesemia  Cause  Reduced renal functions - is a greater-than-normal  Excessive intake or absorption serum concentration of  Too rapid replacement of magnesium magnesium.  Excessive use of magnesium drugs or products  atrial dysrhythmias and heart blocks  Untreated diabetic ketoacidosis  Hyperparathyroidism  ECF volume depletion  Chronic diarrhea Hypermagnesemia (Continued)  Hypermagnesemia (Continued)  Nursing Interventions  Monitor cardiac rate and rhythm  Monitor BP  Encourage coughing and deep breathing exercises  Check patellar reflexes periodically  Encourage increased fluid intake, if appropriate  Promote bedrest  Monitor Intake and output and 24 hour fluid balance  Recommend avoidance of magnesium-containing antacids  Hypophosphatemia Causes  Malnourished patients who receive parenteral nutrition  Below-normal serum  Prolonged intense hyperventilation concentration of  Alcohol withdrawal inorganic phosphorus  Poor dietary intake  DKA  Major thermal burns  Low magnesium level, low potassium, hyperparathyroidism (related to increased urinary losses of phosphorus)  Hypophosphatemia (Continued)  Clinical Manifestations  Irritability,  Fatigue  Apprehension  Weakness  Numbness  Paresthesias,  confusion, seizures, and coma.  Hypophosphatemia (Continued)  Management Severe hypophosphatemia is dangerous and requires prompt attention.  Aggressive IV phosphorus correction is usually limited -to patient serum phosphorus levels below 1mg/dL -whose GI tract is not functioning  Rate of phosphorus administration not exceed 10 mEq/h -site should be monitored (sloughing and necrosis)  Oral phosphorus replacement in less acute  Hypophosphatemia (Continued)  Nursing Interventions  Identify the risk of hypophosphatemia and monitor  Preventive measures involve gradually introducing solution:  to avoid rapid shift of phosphorus into cells  Preventing infection because hypophosphatemia may alter granulocytes  Frequently monitors serum phosphorus level  Encourage patient to include in diet food high in phosphate  Hyperphosphatemia - is a serum phosphorus level that Cause exceeds normal.  Renal failure  Chemotherapy  Hypoparathyroidism  Respiratory acidosis or DKA  High phosphate intake  Profound muscle necrosis  Increased phosphorus absorption CLO1 Achieved  Hyperphosphatemia (Continued)  Clinical Manifestations  Tetany  Tingling sensation  Anorexia  Nausea  Decrease urine output  Vomiting  Impairing vision  Muscle weakness  Palpitations  Hyperreflexia  tachycardia CLO2 Achieved  Hyperphosphatemia (Continued)  Management  Treatment is directed at the underlying disorder Eg. Hyperphosphatemia may be related to  volume depletion or respiratory or metabolic  Low phosphate diet and phosphate binders  Include Vit.D such as calcitol and calcijex  Dialysis  Phosphate-binding gels or antacids CLO4 Achieved  Hyperphosphatemia (Continued)  Nursing Interventions  Monitors patient at risk  Instruct patient to avoid phosphorus-rich foods  Hard cheese, nuts, whole-grain cereals, dried fruits, dried vegetables, sardines, sweetbread, foods made with milk  Instruct the patient to avoid substance such as laxatives and enemas that contain phosphate.  Teach patient to recognize signs of impending hypocalcemia  Monitor urine output CLO4 Achieved  Acid-Base Imbalances Metabolic Acidosis -disturbance characterized by low pH and low plasma HCO3 concentration Causes:  Diarrhea  Lower intestinal fistulas  Use of diuretics  Early renal insufficiency  Excessive administration of Chloride Normal Values:  Administration of parenteral nutrition pH 7.35 to 7.45 without bicarbonate HCO3 22-26 meq/L  Acid-Base Imbalances (continued) Metabolic Alkalosis -disturbances characterized by high pH and high plasma HCO3 concentration Causes:  Vomiting  Gastric suction with loss hydrogen and chloride ions.  Diuretics therapy Normal Values:  Excessive adrenocorticoid hormones pH 7.35 to 7.45 HCO3 22-26 meq/L  Acid-Base Imbalances (continued) Respiratory Acidosis -the pH is less than 7.35 and the PaCO2 is greater than 42 mm Hg. Causes:  Acute pulmonary edema  Aspiration  Atelectasis  Overdose of sedatives  Pneumothorax  Sleep apnea syndrome  Severe pneumonia Normal Values:  Acute respiratory distress syndrome pH 7.35 to 7.45 PaCO2 38-42 mm hg  Acid-Base Imbalances (continued) Respiratory Alkalosis -the arterial pH is greater than 7.45 and the PaCO2 is less that 38 mm Hg. Causes:  Hyperventilation  extreme anxiety  Hypoxemia  Salicylate intoxication  Inappropriate ventilator settings. Normal Values: pH 7.35 to 7.45 PaCO2 38-42 mm hg  Acid-Base Imbalances (continued) Mixed Acid-Based Disorders  Patients can simultaneously experience two or more independent acid–base disorders  Normal pH in the presence of changes in the PaCO2 and plasma HCO3 concentration immediately suggest mixed disorder Example: Simultaneous occurrence of metabolic acidosis and respiratory acidosis during;  Respiratory and Cardiac Arrest  Compensation  Pulmonary and renal systems compensate for each other  to return the pH to normal.  In a single acid–base disorder, the system not causing the problem will try to compensate by returning the ratio of HCO3 to carbonic acid to the normal 20:1.  The lungs compensate for metabolic disturbances by changing CO2 excretion.  The kidneys compensate for respiratory disturbances by altering bicarbonate retention and H+ secretion. Compensation (continued)  Critical Thinking Question No. 1 1. Lab tests revealed that patient sodium is 170 mEq/L. Which clinical manifestation would the nurse to assess? a. Tented skin turgor and thirst b. Muscle twitching and tetany c. Fruity breath and Kussmaul’s respirations d. Muscle weakness and paresthesia 2. Which electrolyte would the nurse identify as the major electrolyte responsible for determining the concentration of the extracellular fluid? a. Phosphate b. Potassium c. Sodium d. Chloride